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Re: [Genetics-Psittacine] Parblues IRN do not exist

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  • Recio Joaquin
    Hi Peter,   You said :   In my opinion it is better to use incomplete dominance as co-dominance is a case when each allele has the full 100% expression
    Message 1 of 27 , Aug 1 12:25 AM
      Hi Peter,
       
      You said :
       "In my opinion it is better to use incomplete dominance as co-dominance is a case when each allele has the full 100% expression without overpower the other. Like in bloodtype AB where both the A type allele and B type allele have full expression"
      I agree Peter. Thank you for the correction :) happy
       
      "This gene pair can not activate itself for 200%. This must be 100%. Mother nature created a second wild allel to repair the errors of pottential mutated counterparts. Fundamentally a wild gene doesn’t need a wild counterpart to activate 100%. For example cin+/y and cin+/cin+ . It will be always 100%."
      We agree : One gene can not be activated more than 100%. When I write more than 100% activation I am meaning "capacity of activation". You say "a wild gene doesn’t need a wild counterpart to activate 100%" .... as I explained in the first part of the post this is not always true. It depends on the type of wild gene. Ex : the wild gene which mutates to produce the grey mutation, is unable to produce the wild phenotype if there is only one copy of the wild allele. This is the same for every wild gene corresponding to every mutation behaving as dominant.
      The second wild allele function is related mainly to the production of individuals with a new genetic make up by a crossingover mechanism typical of diploid living beings. It allows for more genetic and phenotypic diversity, better adaptation and quicker speciation.
       
      "WildMutated: those are call split mutations or heterozygous birds: Since the wild type allel has corrected the errors of the mutated allel."
      The wild type allele dose not correct any error of the mutated allele. Again just have a look to the expression of dominant mutations. The system to repair errors in the copy of the DNA has nothing to do with the capacity fo the wild allele to be expressed.
       
      "MutatedMutated : those are the homozygous birds. They can be homoallelic or heteroallelic:
      To my knowledge the homoallelic and heteroallelic is a condition of heteroallelomorphs. In the homoallelic situation they have a intermedial expression. In the heteroallelic situation the expression goes in to the direction of the wild type.
      It is my understanding that IRN’s behave homoallelic in TurquoiseBlue and IndigoBlue. I’m not sure about AquaBlue. So, Mut-0Mut-80 has a 40% activation"
      For me homoallelic means that both alleles are the same type, and heteroallelic means that both alleles are different.... but may be I am wrong. I am taking the semantic meaning ad hoc. The direction of the phenotypic expression depends on the type of action of the wild gene, that has mutated, in the metabolic pathway: activatory or inhibitory respective to the production of the final effect.
       
      Thank you for your answer Peter
       
      Recio
       
      From: Peter Wouters <wouterscalant@...>
      To: Genetics-Psittacine@yahoogroups.com
      Sent: Tuesday, July 31, 2012 10:14 PM
      Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist

       
      Hi Recio,
       
      Some thoughts.
       
      2. Codominance ... if one wild allele is able to produce less than100% of the final product and more than 0% ... intermedial phenotype (Ex: dom pied .... SF and DF birds are different).
      In my opinion it is better to use incomplete dominance as co-dominance is a case when each allele has the full 100% expression without overpower the other. Like in bloodtype AB where both the A type allele and B type allele have full expression.
       
      WildWild .... 100 + 100 = 200% .... always wild phenotype which is reached at 100% of expression (system saturated)
      This gene pair can not activate itself for 200%. This must be 100%. Mother nature created a second wild allel to repair the errors of pottential mutated counterparts. Fundamentally a wild gene doesn’t need a wild counterpart to activate 100%. For example cin+/y and cin+/cin+ .
      It will be always 100%.
       
      WildMutated: those are call split mutations or heterozygous birds: Since the wild type allel has corrected the errors of the mutated allel.
      WildMut-0 .... 100+0 = 100% .... wild phenotype
      WildMut-20 ..... 100+0 = 100% .... wild phenotype
      WildMut-40 .... 100+0=100% .... wild phenotype
      WildMut-60 .... 100+0 = 100% .... wild phenotype
      WildMut-80 ..... 100+0 = 100% .... wild phenotype
       
      MutatedMutated : those are the homozygous birds. They can be homoallelic or heteroallelic:
      To my knowledge the homoallelic and heteroallelic is a condition of heteroallelomorphs. In the homoallelic situation they have a intermedial expression. In the heteroallelic situation the expression goes in to the direction of the wild type.
      It is my understanding that IRN’s behave homoallelic in TurquoiseBlue and IndigoBlue. I’m not sure about AquaBlue. So, Mut-0Mut-80 has a 40% activation.
       
      Regards
      Peter
       
       
      Sent: Monday, July 30, 2012 11:04 PM
      Subject: [Genetics-Psittacine] Parblues IRN do not exist
       
       
      Hi everybody,
       
      I will try to show that parblues IRN do not exist. I will proceed as usually, so everybody will have the time to digest the information.
       
      In the last months we have reviewed psittacin type, distribution, intensity, hormonal dependency and age dependent expression trying to find out if there are 1 or 2 genes coding for psittacin production in IRN. Now, after discussion with some of you, I think I also have a genetic reason to think that they are two different genes. Let's go:
       
      First basic genetics for better understanding: 
       
      The non mutated gene is the wild gene. Every mutation described can be considered as a multiallelic series of at least two alleles : the mutated form and the wild form. These alleles can combine as follows :
       
      WildWild .... always wild phenotype
      MutatedMutated ... always mutated phenotype
      WildMutated .... the expression depends on the capacity of the Wild gene to produce the final product:
              1. The mutated gene behaves as recessive .... if just one wild allele is enough to produce 100% of the final product... wild phenotype (Ex: lutino mutation .... split lutino).
              2. Codominance ...  if one wild allele is able to produce less than100% of the final product and more than 0% ... intermedial phenotype (Ex: dom pied .... SF and DF birds are different).
              3. The mutated gene behaves as dominant ... if one wild allele is unable to produce any of the final product (0% of final product). The expression of the final product needs the presence of two wild alleles (Ex : grey mutation).
       
      So as you can see the situation of recessivity, codominance and dominance depends on the type of wild gene : if just one wild allele activation is able to saturate the system (obtain the final effect) or not. Thus we are not speaking correctly when we say that a mutation "is dominant or recessive", since this characteristic of dominancy or recessivity is not dependent on the mutated gene but it is dependent on the wild gene. We should say that a mutation behaves as dominant or recessive respective to the wild gene.
       
      We have just analyzed how the system works considering that the mutated gene is not able at all to activate the system, that is it is an inactive allele. Now we will analyse what happens when the mutated gene is able to partially activate the system to get the final product at a lower percentage than the wild allele (<100%) (this is the case of our "parblues" in IRN).
       
      Let's suposse that we have 4 different partial mutations of the wild allele. Let's call them Mut-20, Mut-40, Mut-60 and Mut-80, meaning that each allele is able to partially activate the system at the % numbers expressed. Let's call Mut-0 the mutation unable to activate the system at all (0% of the final product).
       
      Let's see which would be the phenotypes of the different combinations whenever one wild gene is able to produce 100% of the final effect (this is the case of the genes coding for psittacin: wild split blue shows green phenotype):
       
      WildWild .... 100 + 100 = 200% .... always wild phenotype which is reached at 100% of expression (system saturated)
       
      WildMutated: those are call split mutations or heterozygous birds:
          WildMut-0 .... 100+0 = 100% .... wild phenotype
          WildMut-20 ..... 100+20 = 120% .... wild phenotype
          WildMut-40 .... 100+40 = 140% .... wild phenotype
          WildMut-60 .... 100+60 = 160% .... wild phenotype
          WildMut-80 ..... 100+80 = 180% .... wild phenotype
       
      MutatedMutated : those are the homozygous birds. They can be homoallelic or heteroallelic:
          Homoallelic :     Mut-0Mut-0 .... 0+0 = 0% activation .... mutated bird ... no expression of the final product.
                                  Mut-20Mut-20 .... 20+20 = 40% activation .... partial activation at 40%
                                  Mut-40Mut-40 .... 40+40 = 80% activation .... partial activation at 80% 
                                  Mut-60Mut-60 .... 60+60 = 120% ..... since saturation is reached at 100% .... wild phenotype
                                  Mut-80Mut-80 .... 80+80 = 160%  .... again ....  wild phenotype
          Heteroallelic:     Mut-20Mut-0 .... 20+0 = 20% .... partial activation at 20%
                                  Mut-20Mut-40 .... 20+40 = 60% .... partial activation at 60%
                                  Mut-20Mut-60 .... 20+60 = 80% .... partial activation at 80%/ SPAN>
                                  Mut-20Mut-80 ..... 20+80 = 100% .... wild phenotype
                                  Mut-40Mut-60 ..... 40+60 = 100% .... wild phenotype
                                  Mut-60Mut-80 ..... 60+80 = 140% ..... wild phenotype
       
      As you can see we can get the wild phenotype from partial mutations, without any wild allele in the genetic make up of the birds.
       
      For those breeding IRN you can change Mut-0 by Blue, Mut-20 by Saphire, Mut-40 by Indigo, Mut-60 by Light Turquoise and Mut-80 by Heavy Turquoise, but this does not mean that the mutations identified by these morphotypes are the only partial mutations in IRN (we could have a Mut-5, Mut-15, Mut 33, ....).
       
      Time for questions before going further.
       
      Regards
       
      Recio
       


    • Recio Joaquin
      Hi everybody,   Just asking this collateral question before going further:   Could we get a wild type phenotype by the combination in the same bird of an
      Message 2 of 27 , Aug 1 4:43 AM
        Hi everybody,
         
        Just asking this collateral question before going further:
         
        Could we get a wild type phenotype by the combination in the same bird of an homozygous Heavy Turquoise and an homozygous Emerald? The answer is non, because in the homozygous Emerald there is a change in the quality of the psittacine produced. It would be really interesting to have a look at a bird showing the patched psittacin (yellow fluorescence) and the psittacin expressed by Emerald (blue fluorescence) under uv? Chris : could you have a look under uv to the bird in your website? From a theoretical point of view it would allow us to see a bluish brigth fluorescence in the primary flying feathers, and a mixed fluorescence (blue + yellow) throughtout the rest of the body. We would also know how our retina perceives two fluorescent colours together. The bright fluorescence we see is due to the emision of energy when the exited electron returns to its basal state. The emitted energy shows a fixed wavelength, like the monochromatic lasser light, and probably this is the reason of the brigth colour we see. So, when both types of fluorescence are present together, that is two different wavelengths, ... will we see a green fluorescence or will we see a green solid colour? .... or another(s) fluorescent/solid colours dependending on the different amounts of each fluorescent psittacin in every body area? This is a very interesting experiment to do.
         
        If we mix in the same bird a saturated patched mutation and an homozygous Emerald we will get a bird similar to the wild type under indoor lighting because in this lighting conditions the apparent expression of the Emerald psittacin is similar to the apparent expression of the even psittacin (primary flying feathers of Emerino show a yellow colour with an intensity similar to primary flying feathers of lutino) ... but if we put this bird under uv lighting or under sunlight, the differences will become evidents respective to the real wild green bird.
         
        Regards
         
        Recio


        From: Recio Joaquin <jrecio99@...>
        To: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
        Sent: Tuesday, July 31, 2012 10:07 PM
        Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist

         
        Hi everybody,
         
        Since there are not questions I guess that this argument pointing to the existence of two different genes coding for psittacins is validated ... although the only real validation will come from breeding results showing the inheritance pattern of Emerald :) happy. Let's try to go further:
         
        We have seen that the lack of ability to get the wild phenotype in a bird showing >100% expressivity is the prove that there is not just one single gene but, probably, two genes coding for psittacin synthesis.
         
        Following our reasoning we could describe the "patched mutations" as mutations acting differently on two different genes :
        1. Partial activation of the gene coding for patched psittacin expression. In the case of Heavy Turquoise this activation would be maximal (100% for this gene). For the other alleles the partial activation in heterozygous and some homozygous birds, leads to a decrease in the quantity of final normal product (patched psittacin) ... lighter patched phenotypes.
        2. Total inactivation of the gene coding for even psittacin expression.... no psittacine in primary flying feathers and green-bluish body.
         
        And, similarly, Emerald mutation should be described as a mutation acting differently also on two different genes:
        1. Total inactivation of the gene coding for patched psittacin expression.... no patched pattern.
        2. Partial activation of the gene coding for even psittacin expression. This partial activation leads to a change in the type of the final product :change in the type of psittacin, which becomes fluorescent respective to the normal even psittacin which is not fluorescent (primary flying feathers of wild birds are not fluorescent). This fluorescent psittacin (blue) is also different than the fluorescent psittacine expressed by patched mutations (yellow).
         
        As you can see for each mutation type there is a total inactivation of a gene (main effect) and a partial activation of a second gene (secondary effect).
         
        ... and a Blue mutation? How does it work? Blue mutation is able to completely block the expression of both genes:
        1. Total inactivation of the gene coding for patched psittacin (like in Emerald mutation)
        2. Total inactivation of the gene coding for even psittacin (like in patched mutations)
        Thus Blue mutation appears as the addition of saturated patched mutation and Emerald mutation. The main effect of each mutation (gene inactivation) does not allow the expression of the secondary effects (partial activation) of each gene.
         
        This reasoning adepts to Terry's theory of two close genes, probably tween genes, able to interact so that the inactivation of one of them (main effect) is able to change the expression of the second one (secondary effect). This is based in what has been called non allelic non complementation, and has been some time ago clearly explained by Terry (http://pets.dir.groups.yahoo.com/group/Genetics-Psittacine/message/20509). If these two genes are closely related probably they have some common "regulators" (very probably they share a common "ancestor" and thus a common regulation) able to act on both at the same time. Mutations acting on these regulators (Blue mutation?) could explain the inactivation of both genes at the same time (here I am guessing that Deon could treat this subject far better than me). Please Terry and Deon, could you clarify further these ideas?
         
        One question for all of you : could we get a wild phenotype by the combination in the same bird of an homozygous Heavy Turquoise and an homozygous Emerald? You can have a look at a bird supossed to be a phenotypic Turquoise Emerald in Chris website (probably genotypic Heterozygous Turquoise Heterozygous Emerald).
         
        Regards
         
        Recio


        From: Recio Joaquin <jrecio99@...>
        To: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
        Sent: Tuesday, July 31, 2012 4:43 PM
        Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist

         
        Thank you Madas for your answer. You are extremely smart, as always : Why a mutated bird, with more than 100% of alleles expressivity, does not show a wild phenotype? Why an homozygous Heavy Turquoise does not look like a wild bird? This is the good question I was expecting.
         
        The answer to this question is the key point of my reasoning : The homozygous Heavy Turquoise (and any other allele combination showing more than 100% expressivity ... that is: saturating the system) is showing us the wild phenotype of the gene coding for one type of psittacine (the patched psittacine). The lacking psittacine to get the final apparent wild phenotype corresponds to the psittacine produced by the activation of another different gene : the gene coding for the even psittacine. This even psittacin is expressed throughout the whole bird, including the primary flying feathers, and its addition to a saturated patched schema allows to get the final green wild phenotype we all know. This is why we will never get the apparent wild phenotype just by "adding patched partial mutations".
         
        As always ... questions before going on ...
         
        Regards
         
        Recio


        From: Stefan Adam <mada_s@...>
        To: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
        Sent: Tuesday, July 31, 2012 8:03 AM
        Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist

         
        Hi Recio,
         
        interesting thoughts. But there is one mistake within yout theory. If the birds with more then 100% are saturated and showing a wildform phenotype then a homozygous turquoise IRN should have green main flights and green tail. But such a bird is showing blue fligths and tail. See attached pic of Willy which he posted some months (years ;) ) ago. For eyes the "green" wing color is some steps darker then the one of a normal green. I think Willy mentioned it in the past too.
         
        Your thougths???
         
        S. Adam
         
        Von: Recio Joaquin <jrecio99@...>
        An: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
        Gesendet: 23:04 Montag, 30.Juli 2012
        Betreff: [Genetics-Psittacine] Parblues IRN do not exist

         
        Hi everybody,
         
        I will try to show that parblues IRN do not exist. I will proceed as usually, so everybody will have the time to digest the information.
         
        In the last months we have reviewed psittacin type, distribution, intensity, hormonal dependency and age dependent expression trying to find out if there are 1 or 2 genes coding for psittacin production in IRN. Now, after discussion with some of you, I think I also have a genetic reason to think that they are two different genes. Let's go:
         
        First basic genetics for better understanding: 
         
        The non mutated gene is the wild gene. Every mutation described can be considered as a multiallelic series of at least two alleles : the mutated form and the wild form. These alleles can combine as follows :
         
        WildWild .... always wild phenotype
        MutatedMutated ... always mutated phenotype
        WildMutated .... the expression depends on the capacity of the Wild gene to produce the final product:
                1. The mutated gene behaves as recessive .... if just one wild allele is enough to produce 100% of the final product... wild phenotype (Ex: lutino mutation .... split lutino).
                2. Codominance ...  if one wild allele is able to produce less than100% of the final product and more than 0% ... intermedial phenotype (Ex: dom pied .... SF and DF birds are different).
                3. The mutated gene behaves as dominant ... if one wild allele is unable to produce any of the final product (0% of final product). The expression of the final product needs the presence of two wild alleles (Ex : grey mutation).
         
        So as you can see the situation of recessivity, codominance and dominance depends on the type of wild gene : if just one wild allele activation is able to saturate the system (obtain the final effect) or not. Thus we are not speaking correctly when we say that a mutation "is dominant or recessive", since this characteristic of dominancy or recessivity is not dependent on the mutated gene but it is dependent on the wild gene. We should say that a mutation behaves as dominant or recessive respective to the wild gene.
         
        We have just analyzed how the system works considering that the mutated gene is not able at all to activate the system, that is it is an inactive allele. Now we will analyse what happens when the mutated gene is able to partially activate the system to get the final product at a lower percentage than the wild allele (<100%) (this is the case of our "parblues" in IRN).
         
        Let's suposse that we have 4 different partial mutations of the wild allele. Let's call them Mut-20, Mut-40, Mut-60 and Mut-80, meaning that each allele is able to partially activate the system at the % numbers expressed. Let's call Mut-0 the mutation unable to activate the system at all (0% of the final product).
         
        Let's see which would be the phenotypes of the different combinations whenever one wild gene is able to produce 100% of the final effect (this is the case of the genes coding for psittacin: wild split blue shows green phenotype):
         
        WildWild .... 100 + 100 = 200% .... always wild phenotype which is reached at 100% of expression (system saturated)
         
        WildMutated: those are call split mutations or heterozygous birds:
            WildMut-0 .... 100+0 = 100% .... wild phenotype
            WildMut-20 ..... 100+20 = 120% .... wild phenotype
            WildMut-40 .... 100+40 = 140% .... wild phenotype
            WildMut-60 .... 100+60 = 160% .... wild phenotype
            WildMut-80 ..... 100+80 = 180% .... wild phenotype
         
        MutatedMutated : those are the homozygous birds. They can be homoallelic or heteroallelic:
            Homoallelic :     Mut-0Mut-0 .... 0+0 = 0% activation .... mutated bird ... no expression of the final product.
                                    Mut-20Mut-20 .... 20+20 = 40% activation .... partial activation at 40%
                                    Mut-40Mut-40 .... 40+40 = 80% activation .... partial activation at 80%  
                                    Mut-60Mut-60 .... 60+60 = 120% ..... since saturation is reached at 100% .... wild phenotype
                                    Mut-80Mut-80 .... 80+80 = 160%  .... again ....  wild phenotype
            Heteroallelic:     Mut-20Mut-0 .... 20+0 = 20% .... partial activation at 20%
                                    Mut-20Mut-40 .... 20+40 = 60% .... partial activation at 60%
                                    Mut-20Mut-60 .... 20+60 = 80% .... partial activation at 80%
                                    Mut-20Mut-80 ..... 20+80 = 100% .... wild phenotype
                                    Mut-40Mut-60 ..... 40+60 = 100% .... wild phenotype
                                    Mut-60Mut-80 ..... 60+80 = 140% ..... wild phenotype
         
        As you can see we can get the wild phenotype from partial mutations, without any wild allele in the genetic make up of the birds.
         
        For those breeding IRN you can change Mut-0 by Blue, Mut-20 by Saphire, Mut-40 by Indigo, Mut-60 by Light Turquoise and Mut-80 by Heavy Turquoise, but this does not mean that the mutations identified by these morphotypes are the only partial mutations in IRN (we could have a Mut-5, Mut-15, Mut 33, ....).
         
        Time for questions before going further.
         
        Regards
         
        Recio
         








      • Peter Wouters
        Hi Recio, I think I understand what you mean. You are probably reffering to haplosufficiency and haploinsufficiency. But I still do not understand how to get a
        Message 3 of 27 , Aug 1 11:48 AM
          Hi Recio,
           
          I think I understand what you mean. You are probably reffering to haplosufficiency and haploinsufficiency. But I still do not understand how to get a wildtype from mut-60 mut-60.
           
          Regards
          Peter
           
          Sent: Wednesday, August 01, 2012 9:25 AM
          Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
           
           

          Hi Peter,
           
          You said :
          "In my opinion it is better to use incomplete dominance as co-dominance is a case when each allele has the full 100% expression without overpower the other. Like in bloodtype AB where both the A type allele and B type allele have full expression"
          I agree Peter. Thank you for the correction :) happy
           
          "This gene pair can not activate itself for 200%. This must be 100%. Mother nature created a second wild allel to repair the errors of pottential mutated counterparts. Fundamentally a wild gene doesn’t need a wild counterpart to activate 100%. For example cin+/y and cin+/cin+ . It will be always 100%."
          We agree : One gene can not be activated more than 100%. When I write more than 100% activation I am meaning "capacity of activation". You say "a wild gene doesn’t need a wild counterpart to activate 100%" .... as I explained in the first part of the post this is not always true. It depends on the type of wild gene. Ex : the wild gene which mutates to produce the grey mutation, is unable to produce the wild phenotype if there is only one copy of the wild allele. This is the same for every wild gene corresponding to every mutation behaving as dominant.
          The second wild allele function is related mainly to the production of individuals with a new genetic make up by a crossingover mechanism typical of diploid living beings. It allows for more genetic and phenotypic diversity, better adaptation and quicker speciation.
           
          "WildMutated: those are call split mutations or heterozygous birds: Since the wild type allel has corrected the errors of the mutated allel."
          The wild type allele dose not correct any error of the mutated allele. Again just have a look to the expression of dominant mutations. The system to repair errors in the copy of the DNA has nothing to do with the capacity fo the wild allele to be expressed.
           
          "MutatedMutated : those are the homozygous birds. They can be homoallelic or heteroallelic:
          To my knowledge the homoallelic and heteroallelic is a condition of heteroallelomorphs. In the homoallelic situation they have a intermedial expression. In the heteroallelic situation the expression goes in to the direction of the wild type.
          It is my understanding that IRN’s behave homoallelic in TurquoiseBlue and IndigoBlue. I’m not sure about AquaBlue. So, Mut-0Mut-80 has a 40% activation"
          For me homoallelic means that both alleles are the same type, and heteroallelic means that both alleles are different.... but may be I am wrong. I am taking the semantic meaning ad hoc. The direction of the phenotypic expression depends on the type of action of the wild gene, that has mutated, in the metabolic pathway: activatory or inhibitory respective to the production of the final effect.
           
          Thank you for your answer Peter
           
          Recio
           
          From: Peter Wouters <wouterscalant@...>
          To: Genetics-Psittacine@yahoogroups.com
          Sent: Tuesday, July 31, 2012 10:14 PM
          Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
           
           
          Hi Recio,
           
          Some thoughts.
           
          2. Codominance ... if one wild allele is able to produce less than100% of the final product and more than 0% ... intermedial phenotype (Ex: dom pied .... SF and DF birds are different).
          In my opinion it is better to use incomplete dominance as co-dominance is a case when each allele has the full 100% expression without overpower the other. Like in bloodtype AB where both the A type allele and B type allele have full expression.
           
          WildWild .... 100 + 100 = 200% .... always wild phenotype which is reached at 100% of expression (system saturated)
          This gene pair can not activate itself for 200%. This must be 100%. Mother nature created a second wild allel to repair the errors of pottential mutated counterparts. Fundamentally a wild gene doesn’t need a wild counterpart to activate 100%. For example cin+/y and cin+/cin+ .
          It will be always 100%.
           
          WildMutated: those are call split mutations or heterozygous birds: Since the wild type allel has corrected the errors of the mutated allel.
          WildMut-0 .... 100+0 = 100% .... wild phenotype
          WildMut-20 ..... 100+0 = 100% .... wild phenotype
          WildMut-40 .... 100+0=100% .... wild phenotype
          WildMut-60 .... 100+0 = 100% .... wild phenotype
          WildMut-80 ..... 100+0 = 100% .... wild phenotype
           
          MutatedMutated : those are the homozygous birds. They can be homoallelic or heteroallelic:
          To my knowledge the homoallelic and heteroallelic is a condition of heteroallelomorphs. In the homoallelic situation they have a intermedial expression. In the heteroallelic situation the expression goes in to the direction of the wild type.
          It is my understanding that IRN’s behave homoallelic in TurquoiseBlue and IndigoBlue. I’m not sure about AquaBlue. So, Mut-0Mut-80 has a 40% activation.
           
          Regards
          Peter
           
           
          Sent: Monday, July 30, 2012 11:04 PM
          Subject: [Genetics-Psittacine] Parblues IRN do not exist
           
           
          Hi everybody,
           
          I will try to show that parblues IRN do not exist. I will proceed as usually, so everybody will have the time to digest the information.
           
          In the last months we have reviewed psittacin type, distribution, intensity, hormonal dependency and age dependent expression trying to find out if there are 1 or 2 genes coding for psittacin production in IRN. Now, after discussion with some of you, I think I also have a genetic reason to think that they are two different genes. Let's go:
           
          First basic genetics for better understanding: 
           
          The non mutated gene is the wild gene. Every mutation described can be considered as a multiallelic series of at least two alleles : the mutated form and the wild form. These alleles can combine as follows :
           
          WildWild .... always wild phenotype
          MutatedMutated ... always mutated phenotype
          WildMutated .... the expression depends on the capacity of the Wild gene to produce the final product:
                  1. The mutated gene behaves as recessive .... if just one wild allele is enough to produce 100% of the final product... wild phenotype (Ex: lutino mutation .... split lutino).
                  2. Codominance ...  if one wild allele is able to produce less than100% of the final product and more than 0% ... intermedial phenotype (Ex: dom pied .... SF and DF birds are different).
                  3. The mutated gene behaves as dominant ... if one wild allele is unable to produce any of the final product (0% of final product). The expression of the final product needs the presence of two wild alleles (Ex : grey mutation).
           
          So as you can see the situation of recessivity, codominance and dominance depends on the type of wild gene : if just one wild allele activation is able to saturate the system (obtain the final effect) or not. Thus we are not speaking correctly when we say that a mutation "is dominant or recessive", since this characteristic of dominancy or recessivity is not dependent on the mutated gene but it is dependent on the wild gene. We should say that a mutation behaves as dominant or recessive respective to the wild gene.
           
          We have just analyzed how the system works considering that the mutated gene is not able at all to activate the system, that is it is an inactive allele. Now we will analyse what happens when the mutated gene is able to partially activate the system to get the final product at a lower percentage than the wild allele (<100%) (this is the case of our "parblues" in IRN).
           
          Let's suposse that we have 4 different partial mutations of the wild allele. Let's call them Mut-20, Mut-40, Mut-60 and Mut-80, meaning that each allele is able to partially activate the system at the % numbers expressed. Let's call Mut-0 the mutation unable to activate the system at all (0% of the final product).
           
          Let's see which would be the phenotypes of the different combinations whenever one wild gene is able to produce 100% of the final effect (this is the case of the genes coding for psittacin: wild split blue shows green phenotype):
           
          WildWild .... 100 + 100 = 200% .... always wild phenotype which is reached at 100% of expression (system saturated)
           
          WildMutated: those are call split mutations or heterozygous birds:
              WildMut-0 .... 100+0 = 100% .... wild phenotype
              WildMut-20 ..... 100+20 = 120% .... wild phenotype
              WildMut-40 .... 100+40 = 140% .... wild phenotype
              WildMut-60 .... 100+60 = 160% .... wild phenotype
              WildMut-80 ..... 100+80 = 180% .... wild phenotype
           
          MutatedMutated : those are the homozygous birds. They can be homoallelic or heteroallelic:
              Homoallelic :     Mut-0Mut-0 .... 0+0 = 0% activation .... mutated bird ... no expression of the final product.
                                      Mut-20Mut-20 .... 20+20 = 40% activation .... partial activation at 40%
                                      Mut-40Mut-40 .... 40+40 = 80% activation .... partial activation at 80% 
                                      Mut-60Mut-60 .... 60+60 = 120% ..... since saturation is reached at 100% .... wild phenotype
                                      Mut-80Mut-80 .... 80+80 = 160%  .... again ....  wild phenotype
              Heteroallelic:     Mut-20Mut-0 .... 20+0 = 20% .... partial activation at 20%
                                      Mut-20Mut-40 .... 20+40 = 60% .... partial activation at 60%
                                      Mut-20Mut-60 .... 20+60 = 80% .... partial activation at 80%/ SPAN>
                                      Mut-20Mut-80 ..... 20+80 = 100% .... wild phenotype
                                      Mut-40Mut-60 ..... 40+60 = 100% .... wild phenotype
                                      Mut-60Mut-80 ..... 60+80 = 140% ..... wild phenotype
           
          As you can see we can get the wild phenotype from partial mutations, without any wild allele in the genetic make up of the birds.
           
          For those breeding IRN you can change Mut-0 by Blue, Mut-20 by Saphire, Mut-40 by Indigo, Mut-60 by Light Turquoise and Mut-80 by Heavy Turquoise, but this does not mean that the mutations identified by these morphotypes are the only partial mutations in IRN (we could have a Mut-5, Mut-15, Mut 33, ....).
           
          Time for questions before going further.
           
          Regards
           
          Recio
           


        • Recio Joaquin
          Hi Peter,   You could only get a wild bird from Mut-60Mut-60 if these alleles were the alleles of the wild gene. Since experience tells us that this kind of
          Message 4 of 27 , Aug 1 12:07 PM
            Hi Peter,
             
            You could only get a wild bird from Mut-60Mut-60 if these alleles were the alleles of the wild gene. Since experience tells us that this kind of bird looks like a heavy turquoise but not like a wild bird (Mada's post), the conclusion is that these alleles are not the alleles of one unique wild gene coding/regulating for all type of psittacin, but that they are the alleles of a different gene, which shows a "wild phenotype" corresponding to the phenotype of the heavy turquoise. The psittacin lacking to complete the wild phenotype (I think that this is the even psittacine) depends on another gene.
             
            Regards
             
            Recio

            From: Peter Wouters <wouterscalant@...>
            To: Genetics-Psittacine@yahoogroups.com
            Sent: Wednesday, August 1, 2012 8:48 PM
            Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist

             
            Hi Recio,
             
            I think I understand what you mean. You are probably reffering to haplosufficiency and haploinsufficiency. But I still do not understand how to get a wildtype from mut-60 mut-60.
             
            Regards
            Peter
             
            Sent: Wednesday, August 01, 2012 9:25 AM
            Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
             
             
            Hi Peter,
             
            You said :
            "In my opinion it is better to use incomplete dominance as co-dominance is a case when each allele has the full 100% expression without overpower the other. Like in bloodtype AB where both the A type allele and B type allele have full expression"
            I agree Peter. Thank you for the correction :) happy
             
            "This gene pair can not activate itself for 200%. This must be 100%. Mother nature created a second wild allel to repair the errors of pottential mutated counterparts. Fundamentally a wild gene doesn’t need a wild counterpart to activate 100%. For example cin+/y and cin+/cin+ . It will be always 100%."
            We agree : One gene can not be activated more than 100%. When I write more than 100% activation I am meaning "capacity of activation". You say "a wild gene doesn’t need a wild counterpart to activate 100%" .... as I explained in the first part of the post this is not always true. It depends on the type of wild gene. Ex : the wild gene which mutates to produce the grey mutation, is unable to produce the wild phenotype if there is only one copy of the wild allele. This is the same for every wild gene corresponding to every mutation behaving as dominant.
            The second wild allele function is related mainly to the production of individuals with a new genetic make up by a crossingover mechanism typical of diploid living beings. It allows for more genetic and phenotypic diversity, better adaptation and quicker speciation.
             
            "WildMutated: those are call split mutations or heterozygous birds: Since the wild type allel has corrected the errors of the mutated allel."
            The wild type allele dose not correct any error of the mutated allele. Again just have a look to the expression of dominant mutations. The system to repair errors in the copy of the DNA has nothing to do with the capacity fo the wild allele to be expressed.
             
            "MutatedMutated : those are the homozygous birds. They can be homoallelic or heteroallelic:
            To my knowledge the homoallelic and heteroallelic is a condition of heteroallelomorphs. In the homoallelic situation they have a intermedial expression. In the heteroallelic situation the expression goes in to the direction of the wild type.
            It is my understanding that IRN’s behave homoallelic in TurquoiseBlue and IndigoBlue. I’m not sure about AquaBlue. So, Mut-0Mut-80 has a 40% activation"
            For me homoallelic means that both alleles are the same type, and heteroallelic means that both alleles are different.... but may be I am wrong. I am taking the semantic meaning ad hoc. The direction of the phenotypic expression depends on the type of action of the wild gene, that has mutated, in the metabolic pathway: activatory or inhibitory respective to the production of the final effect.
             
            Thank you for your answer Peter
             
            Recio
             
            From: Peter Wouters <wouterscalant@...>
            To: Genetics-Psittacine@yahoogroups.com
            Sent: Tuesday, July 31, 2012 10:14 PM
            Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
             
             
            Hi Recio,
             
            Some thoughts.
             
            2. Codominance ... if one wild allele is able to produce less than100% of the final product and more than 0% ... intermedial phenotype (Ex: dom pied .... SF and DF birds are different).
            In my opinion it is better to use incomplete dominance as co-dominance is a case when each allele has the full 100% expression without overpower the other. Like in bloodtype AB where both the A type allele and B type allele have full expression.
             
            WildWild .... 100 + 100 = 200% .... always wild phenotype which is reached at 100% of expression (system saturated)
            This gene pair can not activate itself for 200%. This must be 100%. Mother nature created a second wild allel to repair the errors of pottential mutated counterparts. Fundamentally a wild gene doesn’t need a wild counterpart to activate 100%. For example cin+/y and cin+/cin+ .
            It will be always 100%.
             
            WildMutated: those are call split mutations or heterozygous birds: Since the wild type allel has corrected the errors of the mutated allel.
            WildMut-0 .... 100+0 = 100% .... wild phenotype
            WildMut-20 ..... 100+0 = 100% .... wild phenotype
            WildMut-40 .... 100+0=100% .... wild phenotype
            WildMut-60 .... 100+0 = 100% .... wild phenotype
            WildMut-80 ..... 100+0 = 100% .... wild phenotype
             
            MutatedMutated : those are the homozygous birds. They can be homoallelic or heteroallelic:
            To my knowledge the homoallelic and heteroallelic is a condition of heteroallelomorphs. In the homoallelic situation they have a intermedial expression. In the heteroallelic situation the expression goes in to the direction of the wild type.
            It is my understanding that IRN’s behave homoallelic in TurquoiseBlue and IndigoBlue. I’m not sure about AquaBlue. So, Mut-0Mut-80 has a 40% activation.
             
            Regards
            Peter
             
             
            Sent: Monday, July 30, 2012 11:04 PM
            Subject: [Genetics-Psittacine] Parblues IRN do not exist
             
             
            Hi everybody,
             
            I will try to show that parblues IRN do not exist. I will proceed as usually, so everybody will have the time to digest the information.
             
            In the last months we have reviewed psittacin type, distribution, intensity, hormonal dependency and age dependent expression trying to find out if there are 1 or 2 genes coding for psittacin production in IRN. Now, after discussion with some of you, I think I also have a genetic reason to think that they are two different genes. Let's go:
             
            First basic genetics for better understanding: 
             
            The non mutated gene is the wild gene. Every mutation described can be considered as a multiallelic series of at least two alleles : the mutated form and the wild form. These alleles can combine as follows :
             
            WildWild .... always wild phenotype
            MutatedMutated ... always mutated phenotype
            WildMutated .... the expression depends on the capacity of the Wild gene to produce the final product:
                    1. The mutated gene behaves as recessive .... if just one wild allele is enough to produce 100% of the final product... wild phenotype (Ex: lutino mutation .... split lutino).
                    2. Codominance ...  if one wild allele is able to produce less than100% of the final product and more than 0% ... intermedial phenotype (Ex: dom pied .... SF and DF birds are different).
                    3. The mutated gene behaves as dominant ... if one wild allele is unable to produce any of the final product (0% of final product). The expression of the final product needs the presence of two wild alleles (Ex : grey mutation).
             
            So as you can see the situation of recessivity, codominance and dominance depends on the type of wild gene : if just one wild allele activation is able to saturate the system (obtain the final effect) or not. Thus we are not speaking correctly when we say that a mutation "is dominant or recessive", since this characteristic of dominancy or recessivity is not dependent on the mutated gene but it is dependent on the wild gene. We should say that a mutation behaves as dominant or recessive respective to the wild gene.
             
            We have just analyzed how the system works considering that the mutated gene is not able at all to activate the system, that is it is an inactive allele. Now we will analyse what happens when the mutated gene is able to partially activate the system to get the final product at a lower percentage than the wild allele (<100%) (this is the case of our "parblues" in IRN).
             
            Let's suposse that we have 4 different partial mutations of the wild allele. Let's call them Mut-20, Mut-40, Mut-60 and Mut-80, meaning that each allele is able to partially activate the system at the % numbers expressed. Let's call Mut-0 the mutation unable to activate the system at all (0% of the final product).
             
            Let's see which would be the phenotypes of the different combinations whenever one wild gene is able to produce 100% of the final effect (this is the case of the genes coding for psittacin: wild split blue shows green phenotype):
             
            WildWild .... 100 + 100 = 200% .... always wild phenotype which is reached at 100% of expression (system saturated)
             
            WildMutated: those are call split mutations or heterozygous birds:
                WildMut-0 .... 100+0 = 100% .... wild phenotype
                WildMut-20 ..... 100+20 = 120% .... wild phenotype
                WildMut-40 .... 100+40 = 140% .... wild phenotype
                WildMut-60 .... 100+60 = 160% .... wild phenotype
                WildMut-80 ..... 100+80 = 180% .... wild phenotype
             
            MutatedMutated : those are the homozygous birds. They can be homoallelic or heteroallelic:
                Homoallelic :     Mut-0Mut-0 .... 0+0 = 0% activation .... mutated bird ... no expression of the final product.
                                        Mut-20Mut-20 .... 20+20 = 40% activation .... partial activation at 40%
                                        Mut-40Mut-40 .... 40+40 = 80% activation .... partial activation at 80% 
                                        Mut-60Mut-60 .... 60+60 = 120% ..... since saturation is reached at 100% .... wild phenotype
                                        Mut-80Mut-80 .... 80+80 = 160%  .... again ....  wild phenotype
                Heteroallelic:     Mut-20Mut-0 .... 20+0 = 20% .... partial activation at 20%
                                        Mut-20Mut-40 .... 20+40 = 60% .... partial activation at 60%
                                        Mut-20Mut-60 .... 20+60 = 80% .... partial activation at 80%/ SPAN>
                                        Mut-20Mut-80 ..... 20+80 = 100% .... wild phenotype
                                        Mut-40Mut-60 ..... 40+60 = 100% .... wild phenotype
                                        Mut-60Mut-80 ..... 60+80 = 140% ..... wild phenotype
             
            As you can see we can get the wild phenotype from partial mutations, without any wild allele in the genetic make up of the birds.
             
            For those breeding IRN you can change Mut-0 by Blue, Mut-20 by Saphire, Mut-40 by Indigo, Mut-60 by Light Turquoise and Mut-80 by Heavy Turquoise, but this does not mean that the mutations identified by these morphotypes are the only partial mutations in IRN (we could have a Mut-5, Mut-15, Mut 33, ....).
             
            Time for questions before going further.
             
            Regards
             
            Recio
             




          • Peter Wouters
            Hi Recio, I think you are now reffering to a heteroallelic relation where the different alleles have gene sequence alterations in different functional areas of
            Message 5 of 27 , Aug 1 12:09 PM
              Hi Recio,
               
              I think you are now reffering to a heteroallelic relation where the different alleles have gene sequence alterations in different functional areas of the gene. Right?
               
              Regards
              Peter
               
              Sent: Tuesday, July 31, 2012 4:43 PM
              Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
               
               

              Thank you Madas for your answer. You are extremely smart, as always : Why a mutated bird, with more than 100% of alleles expressivity, does not show a wild phenotype? Why an homozygous Heavy Turquoise does not look like a wild bird? This is the good question I was expecting.
               
              The answer to this question is the key point of my reasoning : The homozygous Heavy Turquoise (and any other allele combination showing more than 100% expressivity ... that is: saturating the system) is showing us the wild phenotype of the gene coding for one type of psittacine (the patched psittacine). The lacking psittacine to get the final apparent wild phenotype corresponds to the psittacine produced by the activation of another different gene : the gene coding for the even psittacine. This even psittacin is expressed throughout the whole bird, including the primary flying feathers, and its addition to a saturated patched schema allows to get the final green wild phenotype we all know. This is why we will never get the apparent wild phenotype just by "adding patched partial mutations".
               
              As always ... questions before going on ...
               
              Regards
               
              Recio

               
              From: Stefan Adam <mada_s@...>
              To: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
              Sent: Tuesday, July 31, 2012 8:03 AM
              Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
               
               
              Hi Recio,
               
              interesting thoughts. But there is one mistake within yout theory. If the birds with more then 100% are saturated and showing a wildform phenotype then a homozygous turquoise IRN should have green main flights and green tail. But such a bird is showing blue fligths and tail. See attached pic of Willy which he posted some months (years ;) ) ago. For eyes the "green" wing color is some steps darker then the one of a normal green. I think Willy mentioned it in the past too.
               
              Your thougths???
               
              S. Adam
               
              Von: Recio Joaquin <jrecio99@...>
              An: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
              Gesendet: 23:04 Montag, 30.Juli 2012
              Betreff: [Genetics-Psittacine] Parblues IRN do not exist
               
               
              Hi everybody,
               
              I will try to show that parblues IRN do not exist. I will proceed as usually, so everybody will have the time to digest the information.
               
              In the last months we have reviewed psittacin type, distribution, intensity, hormonal dependency and age dependent expression trying to find out if there are 1 or 2 genes coding for psittacin production in IRN. Now, after discussion with some of you, I think I also have a genetic reason to think that they are two different genes. Let's go:
               
              First basic genetics for better understanding: 
               
              The non mutated gene is the wild gene. Every mutation described can be considered as a multiallelic series of at least two alleles : the mutated form and the wild form. These alleles can combine as follows :
               
              WildWild .... always wild phenotype
              MutatedMutated ... always mutated phenotype
              WildMutated .... the expression depends on the capacity of the Wild gene to produce the final product:
                      1. The mutated gene behaves as recessive .... if just one wild allele is enough to produce 100% of the final product... wild phenotype (Ex: lutino mutation .... split lutino).
                      2. Codominance ...  if one wild allele is able to produce less than100% of the final product and more than 0% ... intermedial phenotype (Ex: dom pied .... SF and DF birds are different).
                      3. The mutated gene behaves as dominant ... if one wild allele is unable to produce any of the final product (0% of final product). The expression of the final product needs the presence of two wild alleles (Ex : grey mutation).
               
              So as you can see the situation of recessivity, codominance and dominance depends on the type of wild gene : if just one wild allele activation is able to saturate the system (obtain the final effect) or not. Thus we are not speaking correctly when we say that a mutation "is dominant or recessive", since this characteristic of dominancy or recessivity is not dependent on the mutated gene but it is dependent on the wild gene. We should say that a mutation behaves as dominant or recessive respective to the wild gene.
               
              We have just analyzed how the system works considering that the mutated gene is not able at all to activate the system, that is it is an inactive allele. Now we will analyse what happens when the mutated gene is able to partially activate the system to get the final product at a lower percentage than the wild allele (<100%) (this is the case of our "parblues" in IRN).
               
              Let's suposse that we have 4 different partial mutations of the wild allele. Let's call them Mut-20, Mut-40, Mut-60 and Mut-80, meaning that each allele is able to partially activate the system at the % numbers expressed. Let's call Mut-0 the mutation unable to activate the system at all (0% of the final product).
               
              Let's see which would be the phenotypes of the different combinations whenever one wild gene is able to produce 100% of the final effect (this is the case of the genes coding for psittacin: wild split blue shows green phenotype):
               
              WildWild .... 100 + 100 = 200% .... always wild phenotype which is reached at 100% of expression (system saturated)
               
              WildMutated: those are call split mutations or heterozygous birds:
                  WildMut-0 .... 100+0 = 100% .... wild phenotype
                  WildMut-20 ..... 100+20 = 120% .... wild phenotype
                  WildMut-40 .... 100+40 = 140% .... wild phenotype
                  WildMut-60 .... 100+60 = 160% .... wild phenotype
                  WildMut-80 ..... 100+80 = 180% .... wild phenotype
               
              MutatedMutated : those are the homozygous birds. They can be homoallelic or heteroallelic:
                  Homoallelic :     Mut-0Mut-0 .... 0+0 = 0% activation .... mutated bird ... no expression of the final product.
                                          Mut-20Mut-20 .... 20+20 = 40% activation .... partial activation at 40%
                                          Mut-4 0Mut-40 .... 40+40 = 80% activation .... partial activation at 80% 
                                      < /SPAN>    Mut-60Mut-60 .... 60+60 = 120% ..... since saturation is reached at 100% .... wild phenotype
                                    &nb sp;     Mut-80Mut-80 .... 80+80 = 160%  .... again ....  wild phenotype
                  Heteroallelic:     Mut-20Mut-0 .... 20+0 = 20% .... partial activation at 20%
                                          Mut-20Mut-40 .... 20+40 = 60% .... partial activation at 60%
                                          Mut-20Mut-60 .... 20+60 = 80% .... partial activation at 80%
                                          Mut-20Mut-80 ..... 20+80 = 100% .... wild phenotype
                                          Mut-40Mut-60 ..... 40+60 = 100% .... wild phenotype
                                          Mut-60Mut-80 ..... 60+80 = 140% ..... wild phenotype
               
              As you can see we can get the wild phenotype from partial mutations, without any wild allele in the genetic make up of the birds.
               
              For those breeding IRN you can change Mut-0 by Blue, Mut-20 by Saphire, Mut-40 by Indigo, Mut-60 by Light Turquoise and Mut-80 by Heavy Turquoise, but this does not mean that the mutations identified by these morphotypes are the only partial mutations in IRN (we could have a Mut-5, Mut-15, Mut 33, ....).
               
              Time for questions before going further.
               
              Regards
               
              Recio
               




            • Recio Joaquin
              Hi Peter,   Yes when treating of Mut-60Mut-40, but when treating Mut-60Mut-60 the modified alleles are the same... but in both situations the capacity of
              Message 6 of 27 , Aug 1 12:31 PM
                Hi Peter,
                 
                Yes when treating of Mut-60Mut-40, but when treating Mut-60Mut-60 the modified alleles are the same... but in both situations the capacity of producing the final maximal expression (100%) is the same, and this final maximal expression is the patched heavy turquoise morphotype.
                 
                Recio

                From: Peter Wouters <wouterscalant@...>
                To: Genetics-Psittacine@yahoogroups.com
                Sent: Wednesday, August 1, 2012 9:09 PM
                Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist

                 
                Hi Recio,
                 
                I think you are now reffering to a heteroallelic relation where the different alleles have gene sequence alterations in different functional areas of the gene. Right?
                 
                Regards
                Peter
                 
                Sent: Tuesday, July 31, 2012 4:43 PM
                Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                 
                 
                Thank you Madas for your answer. You are extremely smart, as always : Why a mutated bird, with more than 100% of alleles expressivity, does not show a wild phenotype? Why an homozygous Heavy Turquoise does not look like a wild bird? This is the good question I was expecting.
                 
                The answer to this question is the key point of my reasoning : The homozygous Heavy Turquoise (and any other allele combination showing more than 100% expressivity ... that is: saturating the system) is showing us the wild phenotype of the gene coding for one type of psittacine (the patched psittacine). The lacking psittacine to get the final apparent wild phenotype corresponds to the psittacine produced by the activation of another different gene : the gene coding for the even psittacine. This even psittacin is expressed throughout the whole bird, including the primary flying feathers, and its addition to a saturated patched schema allows to get the final green wild phenotype we all know. This is why we will never get the apparent wild phenotype just by "adding patched partial mutations".
                 
                As always ... questions before going on ...
                 
                Regards
                 
                Recio

                 
                From: Stefan Adam <mada_s@...>
                To: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
                Sent: Tuesday, July 31, 2012 8:03 AM
                Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                 
                 
                Hi Recio,
                 
                interesting thoughts. But there is one mistake within yout theory. If the birds with more then 100% are saturated and showing a wildform phenotype then a homozygous turquoise IRN should have green main flights and green tail. But such a bird is showing blue fligths and tail. See attached pic of Willy which he posted some months (years ;) ) ago. For eyes the "green" wing color is some steps darker then the one of a normal green. I think Willy mentioned it in the past too.
                 
                Your thougths???
                 
                S. Adam
                 
                Von: Recio Joaquin <jrecio99@...>
                An: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
                Gesendet: 23:04 Montag, 30.Juli 2012
                Betreff: [Genetics-Psittacine] Parblues IRN do not exist
                 
                 
                Hi everybody,
                 
                I will try to show that parblues IRN do not exist. I will proceed as usually, so everybody will have the time to digest the information.
                 
                In the last months we have reviewed psittacin type, distribution, intensity, hormonal dependency and age dependent expression trying to find out if there are 1 or 2 genes coding for psittacin production in IRN. Now, after discussion with some of you, I think I also have a genetic reason to think that they are two different genes. Let's go:
                 
                First basic genetics for better understanding: 
                 
                The non mutated gene is the wild gene. Every mutation described can be considered as a multiallelic series of at least two alleles : the mutated form and the wild form. These alleles can combine as follows :
                 
                WildWild .... always wild phenotype
                MutatedMutated ... always mutated phenotype
                WildMutated .... the expression depends on the capacity of the Wild gene to produce the final product:
                        1. The mutated gene behaves as recessive .... if just one wild allele is enough to produce 100% of the final product... wild phenotype (Ex: lutino mutation .... split lutino).
                        2. Codominance ...  if one wild allele is able to produce less than100% of the final product and more than 0% ... intermedial phenotype (Ex: dom pied .... SF and DF birds are different).
                        3. The mutated gene behaves as dominant ... if one wild allele is unable to produce any of the final product (0% of final product). The expression of the final product needs the presence of two wild alleles (Ex : grey mutation).
                 
                So as you can see the situation of recessivity, codominance and dominance depends on the type of wild gene : if just one wild allele activation is able to saturate the system (obtain the final effect) or not. Thus we are not speaking correctly when we say that a mutation "is dominant or recessive", since this characteristic of dominancy or recessivity is not dependent on the mutated gene but it is dependent on the wild gene. We should say that a mutation behaves as dominant or recessive respective to the wild gene.
                 
                We have just analyzed how the system works considering that the mutated gene is not able at all to activate the system, that is it is an inactive allele. Now we will analyse what happens when the mutated gene is able to partially activate the system to get the final product at a lower percentage than the wild allele (<100%) (this is the case of our "parblues" in IRN).
                 
                Let's suposse that we have 4 different partial mutations of the wild allele. Let's call them Mut-20, Mut-40, Mut-60 and Mut-80, meaning that each allele is able to partially activate the system at the % numbers expressed. Let's call Mut-0 the mutation unable to activate the system at all (0% of the final product).
                 
                Let's see which would be the phenotypes of the different combinations whenever one wild gene is able to produce 100% of the final effect (this is the case of the genes coding for psittacin: wild split blue shows green phenotype):
                 
                WildWild .... 100 + 100 = 200% .... always wild phenotype which is reached at 100% of expression (system saturated)
                 
                WildMutated: those are call split mutations or heterozygous birds:
                    WildMut-0 .... 100+0 = 100% .... wild phenotype
                    WildMut-20 ..... 100+20 = 120% .... wild phenotype
                    WildMut-40 .... 100+40 = 140% .... wild phenotype
                    WildMut-60 .... 100+60 = 160% .... wild phenotype
                    WildMut-80 ..... 100+80 = 180% .... wild phenotype
                 
                MutatedMutated : those are the homozygous birds. They can be homoallelic or heteroallelic:
                    Homoallelic :     Mut-0Mut-0 .... 0+0 = 0% activation .... mutated bird ... no expression of the final product.
                                            Mut-20Mut-20 .... 20+20 = 40% activation .... partial activation at 40%
                                            Mut-4 0Mut-40 .... 40+40 = 80% activation .... partial activation at 80% 
                                        < /SPAN>    Mut-60Mut-60 .... 60+60 = 120% ..... since saturation is reached at 100% .... wild phenotype
                                      &nb sp;     Mut-80Mut-80 .... 80+80 = 160%  .... again ....  wild phenotype
                    Heteroallelic:     Mut-20Mut-0 .... 20+0 = 20% .... partial activation at 20%
                                            Mut-20Mut-40 .... 20+40 = 60% .... partial activation at 60%
                                            Mut-20Mut-60 .... 20+60 = 80% .... partial activation at 80%
                                            Mut-20Mut-80 ..... 20+80 = 100% .... wild phenotype
                                            Mut-40Mut-60 ..... 40+60 = 100% .... wild phenotype
                                            Mut-60Mut-80 ..... 60+80 = 140% ..... wild phenotype
                 
                As you can see we can get the wild phenotype from partial mutations, without any wild allele in the genetic make up of the birds.
                 
                For those breeding IRN you can change Mut-0 by Blue, Mut-20 by Saphire, Mut-40 by Indigo, Mut-60 by Light Turquoise and Mut-80 by Heavy Turquoise, but this does not mean that the mutations identified by these morphotypes are the only partial mutations in IRN (we could have a Mut-5, Mut-15, Mut 33, ....).
                 
                Time for questions before going further.
                 
                Regards
                 
                Recio
                 






              • Recio Joaquin
                Hi everybody,   At the beginning of this post I said that parblues do not exist in IRN . I am sure that now you understand what I was meaning: if there is
                Message 7 of 27 , Aug 1 1:09 PM
                  Hi everybody,
                   
                  At the beginning of this post I said that "parblues do not exist in IRN". I am sure that now you understand what I was meaning: if there is not a single blue gene ... there can not be partial mutations of blue. The name we give to a mutation is related to the expressed phenotype. Ex: we call lutino a yellow bird showing a mutation in the metabolic pathway leading to melanin synthesis. So ... how should we call our "parblues":
                   
                  Could it be ... Par-patched .... as the expressed phenotype is the patched psittacin? Since at present we have not identified all the alleles of this category, and that our classification is based on a morphotype basis, I propose to use a % nomenclature as follows:
                  PP-10 = parpatched with 10% of expressed psittacin
                  PP-20 = parpatched with 20% of expressed psittacin ... and so on ... till 80%. At 80% we will assume that the patched psittacin is at saturation. Then we should decide which are the PP-% at which fluorescent psittacin and red psittacin appear, to use them as point marks.
                  Parpatched mutations consist in a change in the quantity of patched psittacin expressed (change in intensity), but there can be mutations acting on patched psittacin by other mechanisms:
                  1. Change in distribution : you all know opaline but probably there are other types. Is the saddleback a compound of dom pied and a parpatched redistributing mutation, is the turquoise bird of Karen & John another type of redistributing mutation (30-07-2012).
                  2. Change in psittacin type : patched mutations show at least 3 types of psittacines (yellow non fluorescent, yellow fluorescent and red). We have arguments to think that the yellow fluorescent psittacine and the red psittacine are produced by a transformation of the yellow non fluorescent psittacine. Are the red birds the result of mutations acting on these transformations? We should expect in the futur an explosion of new mutations on psittacins, since the number of enzymes acting on this pathway and the complexity of its regulation it is becoming apparent. Two years ago we were discussing if there was one or two types of yellow psittacines. Today we know that, just in IRN, there at least 3 yellow psittacines.
                   
                  The only mutation of the even psittacine known to date in IRN is Emerald. It consists in a suppresion of the patched psittacine and a change in the type of psittacine. May be in the futur we will get a mutation looking like Emerald but non fluorescent. In this case we will be able to directly see the non mutated even psittacin (evenino?) .... and may be there will also be mutations acting in the quantity of even psittacin expressed. At this moment, if we get a combo of Indigo (PP-40%) and pareven-40% ... we will be able to speak again of parblues  ;) winking
                   
                  Take these ideas as pure speculation ... till breeding results follow.
                   
                  That's all folks
                   
                  Recio


                  From: Recio Joaquin <jrecio99@...>
                  To: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
                  Sent: Wednesday, August 1, 2012 1:43 PM
                  Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist

                   
                  Hi everybody,
                   
                  Just asking this collateral question before going further:
                   
                  Could we get a wild type phenotype by the combination in the same bird of an homozygous Heavy Turquoise and an homozygous Emerald? The answer is non, because in the homozygous Emerald there is a change in the quality of the psittacine produced. It would be really interesting to have a look at a bird showing the patched psittacin (yellow fluorescence) and the psittacin expressed by Emerald (blue fluorescence) under uv? Chris : could you have a look under uv to the bird in your website? From a theoretical point of view it would allow us to see a bluish brigth fluorescence in the primary flying feathers, and a mixed fluorescence (blue + yellow) throughtout the rest of the body. We would also know how our retina perceives two fluorescent colours together. The bright fluorescence we see is due to the emision of energy when the exited electron returns to its basal state. The emitted energy shows a fixed wavelength, like the monochromatic lasser light, and probably this is the reason of the brigth colour we see. So, when both types of fluorescence are present together, that is two different wavelengths, ... will we see a green fluorescence or will we see a green solid colour? .... or another(s) fluorescent/solid colours dependending on the different amounts of each fluorescent psittacin in every body area? This is a very interesting experiment to do.
                   
                  If we mix in the same bird a saturated patched mutation and an homozygous Emerald we will get a bird similar to the wild type under indoor lighting because in this lighting conditions the apparent expression of the Emerald psittacin is similar to the apparent expression of the even psittacin (primary flying feathers of Emerino show a yellow colour with an intensity similar to primary flying feathers of lutino) ... but if we put this bird under uv lighting or under sunlight, the differences will become evidents respective to the real wild green bird.
                   
                  Regards
                   
                  Recio


                  From: Recio Joaquin <jrecio99@...>
                  To: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
                  Sent: Tuesday, July 31, 2012 10:07 PM
                  Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist

                   
                  Hi everybody,
                   
                  Since there are not questions I guess that this argument pointing to the existence of two different genes coding for psittacins is validated ... although the only real validation will come from breeding results showing the inheritance pattern of Emerald :) happy. Let's try to go further:
                   
                  We have seen that the lack of ability to get the wild phenotype in a bird showing >100% expressivity is the prove that there is not just one single gene but, probably, two genes coding for psittacin synthesis.
                   
                  Following our reasoning we could describe the "patched mutations" as mutations acting differently on two different genes :
                  1. Partial activation of the gene coding for patched psittacin expression. In the case of Heavy Turquoise this activation would be maximal (100% for this gene). For the other alleles the partial activation in heterozygous and some homozygous birds, leads to a decrease in the quantity of final normal product (patched psittacin) ... lighter patched phenotypes.
                  2. Total inactivation of the gene coding for even psittacin expression.... no psittacine in primary flying feathers and green-bluish body.
                   
                  And, similarly, Emerald mutation should be described as a mutation acting differently also on two different genes:
                  1. Total inactivation of the gene coding for patched psittacin expression.... no patched pattern.
                  2. Partial activation of the gene coding for even psittacin expression. This partial activation leads to a change in the type of the final product :change in the type of psittacin, which becomes fluorescent respective to the normal even psittacin which is not fluorescent (primary flying feathers of wild birds are not fluorescent). This fluorescent psittacin (blue) is also different than the fluorescent psittacine expressed by patched mutations (yellow).
                   
                  As you can see for each mutation type there is a total inactivation of a gene (main effect) and a partial activation of a second gene (secondary effect).
                   
                  ... and a Blue mutation? How does it work? Blue mutation is able to completely block the expression of both genes:
                  1. Total inactivation of the gene coding for patched psittacin (like in Emerald mutation)
                  2. Total inactivation of the gene coding for even psittacin (like in patched mutations)
                  Thus Blue mutation appears as the addition of saturated patched mutation and Emerald mutation. The main effect of each mutation (gene inactivation) does not allow the expression of the secondary effects (partial activation) of each gene.
                   
                  This reasoning adepts to Terry's theory of two close genes, probably tween genes, able to interact so that the inactivation of one of them (main effect) is able to change the expression of the second one (secondary effect). This is based in what has been called non allelic non complementation, and has been some time ago clearly explained by Terry (http://pets.dir.groups.yahoo.com/group/Genetics-Psittacine/message/20509). If these two genes are closely related probably they have some common "regulators" (very probably they share a common "ancestor" and thus a common regulation) able to act on both at the same time. Mutations acting on these regulators (Blue mutation?) could explain the inactivation of both genes at the same time (here I am guessing that Deon could treat this subject far better than me). Please Terry and Deon, could you clarify further these ideas?
                   
                  One question for all of you : could we get a wild phenotype by the combination in the same bird of an homozygous Heavy Turquoise and an homozygous Emerald? You can have a look at a bird supossed to be a phenotypic Turquoise Emerald in Chris website (probably genotypic Heterozygous Turquoise Heterozygous Emerald).
                   
                  Regards
                   
                  Recio


                  From: Recio Joaquin <jrecio99@...>
                  To: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
                  Sent: Tuesday, July 31, 2012 4:43 PM
                  Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist

                   
                  Thank you Madas for your answer. You are extremely smart, as always : Why a mutated bird, with more than 100% of alleles expressivity, does not show a wild phenotype? Why an homozygous Heavy Turquoise does not look like a wild bird? This is the good question I was expecting.
                   
                  The answer to this question is the key point of my reasoning : The homozygous Heavy Turquoise (and any other allele combination showing more than 100% expressivity ... that is: saturating the system) is showing us the wild phenotype of the gene coding for one type of psittacine (the patched psittacine). The lacking psittacine to get the final apparent wild phenotype corresponds to the psittacine produced by the activation of another different gene : the gene coding for the even psittacine. This even psittacin is expressed throughout the whole bird, including the primary flying feathers, and its addition to a saturated patched schema allows to get the final green wild phenotype we all know. This is why we will never get the apparent wild phenotype just by "adding patched partial mutations".
                   
                  As always ... questions before going on ...
                   
                  Regards
                   
                  Recio


                  From: Stefan Adam <mada_s@...>
                  To: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
                  Sent: Tuesday, July 31, 2012 8:03 AM
                  Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist

                   
                  Hi Recio,
                   
                  interesting thoughts. But there is one mistake within yout theory. If the birds with more then 100% are saturated and showing a wildform phenotype then a homozygous turquoise IRN should have green main flights and green tail. But such a bird is showing blue fligths and tail. See attached pic of Willy which he posted some months (years ;) ) ago. For eyes the "green" wing color is some steps darker then the one of a normal green. I think Willy mentioned it in the past too.
                   
                  Your thougths???
                   
                  S. Adam
                   
                  Von: Recio Joaquin <jrecio99@...>
                  An: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
                  Gesendet: 23:04 Montag, 30.Juli 2012
                  Betreff: [Genetics-Psittacine] Parblues IRN do not exist

                   
                  Hi everybody,
                   
                  I will try to show that parblues IRN do not exist. I will proceed as usually, so everybody will have the time to digest the information.
                   
                  In the last months we have reviewed psittacin type, distribution, intensity, hormonal dependency and age dependent expression trying to find out if there are 1 or 2 genes coding for psittacin production in IRN. Now, after discussion with some of you, I think I also have a genetic reason to think that they are two different genes. Let's go:
                   
                  First basic genetics for better understanding: 
                   
                  The non mutated gene is the wild gene. Every mutation described can be considered as a multiallelic series of at least two alleles : the mutated form and the wild form. These alleles can combine as follows :
                   
                  WildWild .... always wild phenotype
                  MutatedMutated ... always mutated phenotype
                  WildMutated .... the expression depends on the capacity of the Wild gene to produce the final product:
                          1. The mutated gene behaves as recessive .... if just one wild allele is enough to produce 100% of the final product... wild phenotype (Ex: lutino mutation .... split lutino).
                          2. Codominance ...  if one wild allele is able to produce less than100% of the final product and more than 0% ... intermedial phenotype (Ex: dom pied .... SF and DF birds are different).
                          3. The mutated gene behaves as dominant ... if one wild allele is unable to produce any of the final product (0% of final product). The expression of the final product needs the presence of two wild alleles (Ex : grey mutation).
                   
                  So as you can see the situation of recessivity, codominance and dominance depends on the type of wild gene : if just one wild allele activation is able to saturate the system (obtain the final effect) or not. Thus we are not speaking correctly when we say that a mutation "is dominant or recessive", since this characteristic of dominancy or recessivity is not dependent on the mutated gene but it is dependent on the wild gene. We should say that a mutation behaves as dominant or recessive respective to the wild gene.
                   
                  We have just analyzed how the system works considering that the mutated gene is not able at all to activate the system, that is it is an inactive allele. Now we will analyse what happens when the mutated gene is able to partially activate the system to get the final product at a lower percentage than the wild allele (<100%) (this is the case of our "parblues" in IRN).
                   
                  Let's suposse that we have 4 different partial mutations of the wild allele. Let's call them Mut-20, Mut-40, Mut-60 and Mut-80, meaning that each allele is able to partially activate the system at the % numbers expressed. Let's call Mut-0 the mutation unable to activate the system at all (0% of the final product).
                   
                  Let's see which would be the phenotypes of the different combinations whenever one wild gene is able to produce 100% of the final effect (this is the case of the genes coding for psittacin: wild split blue shows green phenotype):
                   
                  WildWild .... 100 + 100 = 200% .... always wild phenotype which is reached at 100% of expression (system saturated)
                   
                  WildMutated: those are call split mutations or heterozygous birds:
                      WildMut-0 .... 100+0 = 100% .... wild phenotype
                      WildMut-20 ..... 100+20 = 120% .... wild phenotype
                      WildMut-40 .... 100+40 = 140% .... wild phenotype
                      WildMut-60 .... 100+60 = 160% .... wild phenotype
                      WildMut-80 ..... 100+80 = 180% .... wild phenotype
                   
                  MutatedMutated : those are the homozygous birds. They can be homoallelic or heteroallelic:
                      Homoallelic :     Mut-0Mut-0 .... 0+0 = 0% activation .... mutated bird ... no expression of the final product.
                                              Mut-20Mut-20 .... 20+20 = 40% activation .... partial activation at 40%
                                              Mut-40Mut-40 .... 40+40 = 80% activation .... partial activation at 80%  
                                              Mut-60Mut-60 .... 60+60 = 120% ..... since saturation is reached at 100% .... wild phenotype
                                              Mut-80Mut-80 .... 80+80 = 160%  .... again ....  wild phenotype
                      Heteroallelic:     Mut-20Mut-0 .... 20+0 = 20% .... partial activation at 20%
                                              Mut-20Mut-40 .... 20+40 = 60% .... partial activation at 60%
                                              Mut-20Mut-60 .... 20+60 = 80% .... partial activation at 80%
                                              Mut-20Mut-80 ..... 20+80 = 100% .... wild phenotype
                                              Mut-40Mut-60 ..... 40+60 = 100% .... wild phenotype
                                              Mut-60Mut-80 ..... 60+80 = 140% ..... wild phenotype
                   
                  As you can see we can get the wild phenotype from partial mutations, without any wild allele in the genetic make up of the birds.
                   
                  For those breeding IRN you can change Mut-0 by Blue, Mut-20 by Saphire, Mut-40 by Indigo, Mut-60 by Light Turquoise and Mut-80 by Heavy Turquoise, but this does not mean that the mutations identified by these morphotypes are the only partial mutations in IRN (we could have a Mut-5, Mut-15, Mut 33, ....).
                   
                  Time for questions before going further.
                   
                  Regards
                   
                  Recio
                   










                • Recio Joaquin
                  Hi Peter,   I will take some definitions from an old post of Terry:           Homozygous means that the two genes on each of a chromosome pair are
                  Message 8 of 27 , Aug 3 8:05 AM
                    Hi Peter,
                     
                    I will take some definitions from an old post of Terry:
                     
                            Homozygous means that the two genes on each of a chromosome pair are the same.
                     
                            Heterozygous means they are each different within the pair
                     
                            Heteroallelic refers to two different mutant alleles and how they relate to each other (not whether they are present together or separate). It implies that they have gene sequence alterations in different functional areas of the gene, so that their effects do not in effect overlap as we see for standard co-dominant alleles.
                     
                            Homoallelic implies that two mutant alleles have alterations in the same functional area of the gene, and therefore behave as differing degrees of the same effect. Virtually all mutant alleles in birds behave in this way. Combine Pallid and Ino and you get an intermediate phenotype. Same happens with Greywing and Clearwing in Budgies, Pastel and NSL Ino in Lovebirds, etc.
                     
                            Parblue mutations have always been the exception in some species and this was initially explained by Peter Bergman using this concept of heteroallelic complementation. In effect it is indicating that the two different alleles have alterations to different functions, which can easily imply they are two different loci.
                     
                            The problem is the use and confusion over the terms heteroallele and homoallele. Stick to heterozygous and homozygous.
                     
                            As for SF parblue, this is a Green bird with one wildtype allele and one parblue allele. Whilst its use persists breeders will continue to think Parblue is dominant and masked by wildtype. To maintain that it doesn't matter because these breeders never mate Parblue x Green is like saying its OK to believe the world is flat because I am never taking a trip out of my country. It is all about a better understanding of the bigger picture, with each fact being an important pre-requisite for further learning. If someone doesn't want to learn, it doesn't matter what terms they use. But then they should not complain that they cannot understand the topic or maintain that they know what they are talking about. Or complain about name changes to mutations for that matter.
                     
                    Considering these definitions the alleles of patched mutations (saphire, indigo, turquoise, ...) should be considered as homoallelic... but when I am treating of patched mutations respective to even mutation I am refering to different genes and not to an heteroallelic relation. I think that this is what Peter was refering to. Isn't it?
                     
                    Anyway, time will tell us.
                     
                    Regards
                     
                    Recio

                    From: Peter Wouters <wouterscalant@...>
                    To: Genetics-Psittacine@yahoogroups.com
                    Sent: Wednesday, August 1, 2012 9:09 PM
                    Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist

                     
                    Hi Recio,
                     
                    I think you are now reffering to a heteroallelic relation where the different alleles have gene sequence alterations in different functional areas of the gene. Right?
                     
                    Regards
                    Peter
                     
                    Sent: Tuesday, July 31, 2012 4:43 PM
                    Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                     
                     
                    Thank you Madas for your answer. You are extremely smart, as always : Why a mutated bird, with more than 100% of alleles expressivity, does not show a wild phenotype? Why an homozygous Heavy Turquoise does not look like a wild bird? This is the good question I was expecting.
                     
                    The answer to this question is the key point of my reasoning : The homozygous Heavy Turquoise (and any other allele combination showing more than 100% expressivity ... that is: saturating the system) is showing us the wild phenotype of the gene coding for one type of psittacine (the patched psittacine). The lacking psittacine to get the final apparent wild phenotype corresponds to the psittacine produced by the activation of another different gene : the gene coding for the even psittacine. This even psittacin is expressed throughout the whole bird, including the primary flying feathers, and its addition to a saturated patched schema allows to get the final green wild phenotype we all know. This is why we will never get the apparent wild phenotype just by "adding patched partial mutations".
                     
                    As always ... questions before going on ...
                     
                    Regards
                     
                    Recio

                     
                    From: Stefan Adam <mada_s@...>
                    To: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
                    Sent: Tuesday, July 31, 2012 8:03 AM
                    Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                     
                     
                    Hi Recio,
                     
                    interesting thoughts. But there is one mistake within yout theory. If the birds with more then 100% are saturated and showing a wildform phenotype then a homozygous turquoise IRN should have green main flights and green tail. But such a bird is showing blue fligths and tail. See attached pic of Willy which he posted some months (years ;) ) ago. For eyes the "green" wing color is some steps darker then the one of a normal green. I think Willy mentioned it in the past too.
                     
                    Your thougths???
                     
                    S. Adam
                     
                    Von: Recio Joaquin <jrecio99@...>
                    An: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
                    Gesendet: 23:04 Montag, 30.Juli 2012
                    Betreff: [Genetics-Psittacine] Parblues IRN do not exist
                     
                     
                    Hi everybody,
                     
                    I will try to show that parblues IRN do not exist. I will proceed as usually, so everybody will have the time to digest the information.
                     
                    In the last months we have reviewed psittacin type, distribution, intensity, hormonal dependency and age dependent expression trying to find out if there are 1 or 2 genes coding for psittacin production in IRN. Now, after discussion with some of you, I think I also have a genetic reason to think that they are two different genes. Let's go:
                     
                    First basic genetics for better understanding: 
                     
                    The non mutated gene is the wild gene. Every mutation described can be considered as a multiallelic series of at least two alleles : the mutated form and the wild form. These alleles can combine as follows :
                     
                    WildWild .... always wild phenotype
                    MutatedMutated ... always mutated phenotype
                    WildMutated .... the expression depends on the capacity of the Wild gene to produce the final product:
                            1. The mutated gene behaves as recessive .... if just one wild allele is enough to produce 100% of the final product... wild phenotype (Ex: lutino mutation .... split lutino).
                            2. Codominance ...  if one wild allele is able to produce less than100% of the final product and more than 0% ... intermedial phenotype (Ex: dom pied .... SF and DF birds are different).
                            3. The mutated gene behaves as dominant ... if one wild allele is unable to produce any of the final product (0% of final product). The expression of the final product needs the presence of two wild alleles (Ex : grey mutation).
                     
                    So as you can see the situation of recessivity, codominance and dominance depends on the type of wild gene : if just one wild allele activation is able to saturate the system (obtain the final effect) or not. Thus we are not speaking correctly when we say that a mutation "is dominant or recessive", since this characteristic of dominancy or recessivity is not dependent on the mutated gene but it is dependent on the wild gene. We should say that a mutation behaves as dominant or recessive respective to the wild gene.
                     
                    We have just analyzed how the system works considering that the mutated gene is not able at all to activate the system, that is it is an inactive allele. Now we will analyse what happens when the mutated gene is able to partially activate the system to get the final product at a lower percentage than the wild allele (<100%) (this is the case of our "parblues" in IRN).
                     
                    Let's suposse that we have 4 different partial mutations of the wild allele. Let's call them Mut-20, Mut-40, Mut-60 and Mut-80, meaning that each allele is able to partially activate the system at the % numbers expressed. Let's call Mut-0 the mutation unable to activate the system at all (0% of the final product).
                     
                    Let's see which would be the phenotypes of the different combinations whenever one wild gene is able to produce 100% of the final effect (this is the case of the genes coding for psittacin: wild split blue shows green phenotype):
                     
                    WildWild .... 100 + 100 = 200% .... always wild phenotype which is reached at 100% of expression (system saturated)
                     
                    WildMutated: those are call split mutations or heterozygous birds:
                        WildMut-0 .... 100+0 = 100% .... wild phenotype
                        WildMut-20 ..... 100+20 = 120% .... wild phenotype
                        WildMut-40 .... 100+40 = 140% .... wild phenotype
                        WildMut-60 .... 100+60 = 160% .... wild phenotype
                        WildMut-80 ..... 100+80 = 180% .... wild phenotype
                     
                    MutatedMutated : those are the homozygous birds. They can be homoallelic or heteroallelic:
                        Homoallelic :     Mut-0Mut-0 .... 0+0 = 0% activation .... mutated bird ... no expression of the final product.
                                                Mut-20Mut-20 .... 20+20 = 40% activation .... partial activation at 40%
                                                Mut-4 0Mut-40 .... 40+40 = 80% activation .... partial activation at 80% 
                                            < /SPAN>    Mut-60Mut-60 .... 60+60 = 120% ..... since saturation is reached at 100% .... wild phenotype
                                          &nb sp;     Mut-80Mut-80 .... 80+80 = 160%  .... again ....  wild phenotype
                        Heteroallelic:     Mut-20Mut-0 .... 20+0 = 20% .... partial activation at 20%
                                                Mut-20Mut-40 .... 20+40 = 60% .... partial activation at 60%
                                                Mut-20Mut-60 .... 20+60 = 80% .... partial activation at 80%
                                                Mut-20Mut-80 ..... 20+80 = 100% .... wild phenotype
                                                Mut-40Mut-60 ..... 40+60 = 100% .... wild phenotype
                                                Mut-60Mut-80 ..... 60+80 = 140% ..... wild phenotype
                     
                    As you can see we can get the wild phenotype from partial mutations, without any wild allele in the genetic make up of the birds.
                     
                    For those breeding IRN you can change Mut-0 by Blue, Mut-20 by Saphire, Mut-40 by Indigo, Mut-60 by Light Turquoise and Mut-80 by Heavy Turquoise, but this does not mean that the mutations identified by these morphotypes are the only partial mutations in IRN (we could have a Mut-5, Mut-15, Mut 33, ....).
                     
                    Time for questions before going further.
                     
                    Regards
                     
                    Recio
                     






                  • Recio Joaquin
                    Peter, Deon, Terry, Wynand, .... every other with knowledge in the smart stuff ,   I have checked that the definitions of homoalleles and heteroalleles made
                    Message 9 of 27 , Aug 4 3:52 AM
                      Peter, Deon, Terry, Wynand, .... every other with knowledge in "the smart stuff",
                       
                      I have checked that the definitions of homoalleles and heteroalleles made by Terry are correct... but I have a problem for understanding it : it seems that the changes in nucleotide composition in one specific part of a gene will always produce a change in the quantity of the RNAm produced ... a change in the quantity of the protein produced ... a quantitatif change in the final effect we see .... but changes in a different part of the same gene will finally produce,  by a similar mechanisms, quantitatif changes in a different final effect that we see. In fact it seems that those heteroalleles act as if they were consecutive genes, but, I guess, without a stop codon. Is it the case? If it is the case ... how can we make the difference between two extremely linked genes and two heteroalleles? ... and which would be the functional differences allowing for identification of one or another?
                       
                      First problem : most of the proteins involved in colour regulation are enzymes. The activity of enzymes is highly dependent on its tridimensional structure, and this structure depends mainly on the disposition of some specific aminoacids (those showing an asymetric -NH3 or -COOH), hydrogen bridges, ... that is, on the repartition of electric charges. A change in just one aminoacid can completely change the tridimensional structure of the enzyme and, thus, its activity. We can have different mutations acting at the same point of the gene. Some of them will be able to induce little changes, if any, in the final expression allowing for a change in the quantitatif final effect (classical homoalleles), but others, acting on the same point could induce a big change in the spatial configuration allowing the production of a different enzyme with or without a functional activity. So the same point of the same gene could produce apparent homoalleles and heteroalleles.
                       
                      Second problem: In the same way I can imagine that mutations acting in different parts of the same gene, could lead to a similar final tridimensional structure of the enzyme, producing just a little change in the quantitatif production of the final effect, as if both mutations were homoallelic, despite that they are acting on different points of the same gene.
                       
                      So, how can we say if two alleles behave as homoalleles or as heteroalleles without genetic studies? Which are the criteria to assume one or the other?
                       
                      Regards
                       
                      Recio

                      From: Recio Joaquin <jrecio99@...>
                      To: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
                      Sent: Friday, August 3, 2012 5:05 PM
                      Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist

                       
                      Hi Peter,
                       
                      I will take some definitions from an old post of Terry:
                       
                              Homozygous means that the two genes on each of a chromosome pair are the same.
                       
                              Heterozygous means they are each different within the pair
                       
                              Heteroallelic refers to two different mutant alleles and how they relate to each other (not whether they are present together or separate). It implies that they have gene sequence alterations in different functional areas of the gene, so that their effects do not in effect overlap as we see for standard co-dominant alleles.
                       
                              Homoallelic implies that two mutant alleles have alterations in the same functional area of the gene, and therefore behave as differing degrees of the same effect. Virtually all mutant alleles in birds behave in this way. Combine Pallid and Ino and you get an intermediate phenotype. Same happens with Greywing and Clearwing in Budgies, Pastel and NSL Ino in Lovebirds, etc.
                       
                              Parblue mutations have always been the exception in some species and this was initially explained by Peter Bergman using this concept of heteroallelic complementation. In effect it is indicating that the two different alleles have alterations to different functions, which can easily imply they are two different loci.
                       
                              The problem is the use and confusion over the terms heteroallele and homoallele. Stick to heterozygous and homozygous.
                       
                              As for SF parblue, this is a Green bird with one wildtype allele and one parblue allele. Whilst its use persists breeders will continue to think Parblue is dominant and masked by wildtype. To maintain that it doesn't matter because these breeders never mate Parblue x Green is like saying its OK to believe the world is flat because I am never taking a trip out of my country. It is all about a better understanding of the bigger picture, with each fact being an important pre-requisite for further learning. If someone doesn't want to learn, it doesn't matter what terms they use. But then they should not complain that they cannot understand the topic or maintain that they know what they are talking about. Or complain about name changes to mutations for that matter.
                       
                      Considering these definitions the alleles of patched mutations (saphire, indigo, turquoise, ...) should be considered as homoallelic... but when I am treating of patched mutations respective to even mutation I am refering to different genes and not to an heteroallelic relation. I think that this is what Peter was refering to. Isn't it?
                       
                      Anyway, time will tell us.
                       
                      Regards
                       
                      Recio

                      From: Peter Wouters <wouterscalant@...>
                      To: Genetics-Psittacine@yahoogroups.com
                      Sent: Wednesday, August 1, 2012 9:09 PM
                      Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist

                       
                      Hi Recio,
                       
                      I think you are now reffering to a heteroallelic relation where the different alleles have gene sequence alterations in different functional areas of the gene. Right?
                       
                      Regards
                      Peter
                       
                      Sent: Tuesday, July 31, 2012 4:43 PM
                      Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                       
                       
                      Thank you Madas for your answer. You are extremely smart, as always : Why a mutated bird, with more than 100% of alleles expressivity, does not show a wild phenotype? Why an homozygous Heavy Turquoise does not look like a wild bird? This is the good question I was expecting.
                       
                      The answer to this question is the key point of my reasoning : The homozygous Heavy Turquoise (and any other allele combination showing more than 100% expressivity ... that is: saturating the system) is showing us the wild phenotype of the gene coding for one type of psittacine (the patched psittacine). The lacking psittacine to get the final apparent wild phenotype corresponds to the psittacine produced by the activation of another different gene : the gene coding for the even psittacine. This even psittacin is expressed throughout the whole bird, including the primary flying feathers, and its addition to a saturated patched schema allows to get the final green wild phenotype we all know. This is why we will never get the apparent wild phenotype just by "adding patched partial mutations".
                       
                      As always ... questions before going on ...
                       
                      Regards
                       
                      Recio

                       
                      From: Stefan Adam <mada_s@...>
                      To: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
                      Sent: Tuesday, July 31, 2012 8:03 AM
                      Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                       
                       
                      Hi Recio,
                       
                      interesting thoughts. But there is one mistake within yout theory. If the birds with more then 100% are saturated and showing a wildform phenotype then a homozygous turquoise IRN should have green main flights and green tail. But such a bird is showing blue fligths and tail. See attached pic of Willy which he posted some months (years ;) ) ago. For eyes the "green" wing color is some steps darker then the one of a normal green. I think Willy mentioned it in the past too.
                       
                      Your thougths???
                       
                      S. Adam
                       
                      Von: Recio Joaquin <jrecio99@...>
                      An: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
                      Gesendet: 23:04 Montag, 30.Juli 2012
                      Betreff: [Genetics-Psittacine] Parblues IRN do not exist
                       
                       
                      Hi everybody,
                       
                      I will try to show that parblues IRN do not exist. I will proceed as usually, so everybody will have the time to digest the information.
                       
                      In the last months we have reviewed psittacin type, distribution, intensity, hormonal dependency and age dependent expression trying to find out if there are 1 or 2 genes coding for psittacin production in IRN. Now, after discussion with some of you, I think I also have a genetic reason to think that they are two different genes. Let's go:
                       
                      First basic genetics for better understanding: 
                       
                      The non mutated gene is the wild gene. Every mutation described can be considered as a multiallelic series of at least two alleles : the mutated form and the wild form. These alleles can combine as follows :
                       
                      WildWild .... always wild phenotype
                      MutatedMutated ... always mutated phenotype
                      WildMutated .... the expression depends on the capacity of the Wild gene to produce the final product:
                              1. The mutated gene behaves as recessive .... if just one wild allele is enough to produce 100% of the final product... wild phenotype (Ex: lutino mutation .... split lutino).
                              2. Codominance ...  if one wild allele is able to produce less than100% of the final product and more than 0% ... intermedial phenotype (Ex: dom pied .... SF and DF birds are different).
                              3. The mutated gene behaves as dominant ... if one wild allele is unable to produce any of the final product (0% of final product). The expression of the final product needs the presence of two wild alleles (Ex : grey mutation).
                       
                      So as you can see the situation of recessivity, codominance and dominance depends on the type of wild gene : if just one wild allele activation is able to saturate the system (obtain the final effect) or not. Thus we are not speaking correctly when we say that a mutation "is dominant or recessive", since this characteristic of dominancy or recessivity is not dependent on the mutated gene but it is dependent on the wild gene. We should say that a mutation behaves as dominant or recessive respective to the wild gene.
                       
                      We have just analyzed how the system works considering that the mutated gene is not able at all to activate the system, that is it is an inactive allele. Now we will analyse what happens when the mutated gene is able to partially activate the system to get the final product at a lower percentage than the wild allele (<100%) (this is the case of our "parblues" in IRN).
                       
                      Let's suposse that we have 4 different partial mutations of the wild allele. Let's call them Mut-20, Mut-40, Mut-60 and Mut-80, meaning that each allele is able to partially activate the system at the % numbers expressed. Let's call Mut-0 the mutation unable to activate the system at all (0% of the final product).
                       
                      Let's see which would be the phenotypes of the different combinations whenever one wild gene is able to produce 100% of the final effect (this is the case of the genes coding for psittacin: wild split blue shows green phenotype):
                       
                      WildWild .... 100 + 100 = 200% .... always wild phenotype which is reached at 100% of expression (system saturated)
                       
                      WildMutated: those are call split mutations or heterozygous birds:
                          WildMut-0 .... 100+0 = 100% .... wild phenotype
                          WildMut-20 ..... 100+20 = 120% .... wild phenotype
                          WildMut-40 .... 100+40 = 140% .... wild phenotype
                          WildMut-60 .... 100+60 = 160% .... wild phenotype
                          WildMut-80 ..... 100+80 = 180% .... wild phenotype
                       
                      MutatedMutated : those are the homozygous birds. They can be homoallelic or heteroallelic:
                          Homoallelic :     Mut-0Mut-0 .... 0+0 = 0% activation .... mutated bird ... no expression of the final product.
                                                  Mut-20Mut-20 .... 20+20 = 40% activation .... partial activation at 40%
                                                  Mut-4 0Mut-40 .... 40+40 = 80% activation .... partial activation at 80% 
                                              < /SPAN>    Mut-60Mut-60 .... 60+60 = 120% ..... since saturation is reached at 100% .... wild phenotype
                                            &nb sp;     Mut-80Mut-80 .... 80+80 = 160%  .... again ....  wild phenotype
                          Heteroallelic:     Mut-20Mut-0 .... 20+0 = 20% .... partial activation at 20%
                                                  Mut-20Mut-40 .... 20+40 = 60% .... partial activation at 60%
                                                  Mut-20Mut-60 .... 20+60 = 80% .... partial activation at 80%
                                                  Mut-20Mut-80 ..... 20+80 = 100% .... wild phenotype
                                                  Mut-40Mut-60 ..... 40+60 = 100% .... wild phenotype
                                                  Mut-60Mut-80 ..... 60+80 = 140% ..... wild phenotype
                       
                      As you can see we can get the wild phenotype from partial mutations, without any wild allele in the genetic make up of the birds.
                       
                      For those breeding IRN you can change Mut-0 by Blue, Mut-20 by Saphire, Mut-40 by Indigo, Mut-60 by Light Turquoise and Mut-80 by Heavy Turquoise, but this does not mean that the mutations identified by these morphotypes are the only partial mutations in IRN (we could have a Mut-5, Mut-15, Mut 33, ....).
                       
                      Time for questions before going further.
                       
                      Regards
                       
                      Recio
                       








                    • Deon Smith
                      We are trying to align natural events within boundaries/divisions we have created, instead of the other way round. This all in an effort to understand things
                      Message 10 of 27 , Aug 4 5:34 AM
                        We are trying to align natural events within boundaries/divisions we have created, instead of the other way round. This all in an effort to understand things according to present knowledge.
                        What we have seen lately, is the fading of man-made boundaries in established man-made classification systems with the advances in and release of knowledge. As an example, look at the definitions for inheritance behaviour; dominant, recessive etc. We live in a changing world and so we have to adapt and start thinking about the inadequacies of established systems and start formulating new criteria and new directions of thinking, considering what we know today and what we believe we know.
                         
                        A homozygotic parblue can never be phenotypically wild-type. Even with 80% psittacin loss in a homoallelic homozygous event, there is still a 20% loss of...exactly what? Quantitative decrease of psittacins as a collective homogenous mass of different psittacins? What about the quality, where are the control points for facets of psittacins; colour tone, brilliance, hue, interactions, all the possible modifications, the millions of available colour expressions. The exchange of one metal molecule for another in the white paper for colour production, brought about by a single base substitution and the major effect of such a minute alteration.
                         
                        Deon
                         
                        Sent: Saturday, August 04, 2012 12:52 PM
                        Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                         
                         

                        Peter, Deon, Terry, Wynand, .... every other with knowledge in "the smart stuff",
                         
                        I have checked that the definitions of homoalleles and heteroalleles made by Terry are correct... but I have a problem for understanding it : it seems that the changes in nucleotide composition in one specific part of a gene will always produce a change in the quantity of the RNAm produced ... a change in the quantity of the protein produced ... a quantitatif change in the final effect we see .... but changes in a different part of the same gene will finally produce,  by a similar mechanisms, quantitatif changes in a different final effect that we see. In fact it seems that those heteroalleles act as if they were consecutive genes, but, I guess, without a stop codon. Is it the case? If it is the case ... how can we make the difference between two extremely linked genes and two heteroalleles? ... and which would be the functional differences allowing for identification of one or another?
                         
                        First problem : most of the proteins involved in colour regulation are enzymes. The activity of enzymes is highly dependent on its tridimensional structure, and this structure depends mainly on the disposition of some specific aminoacids (those showing an asymetric -NH3 or -COOH), hydrogen bridges, ... that is, on the repartition of electric charges. A change in just one aminoacid can completely change the tridimensional structure of the enzyme and, thus, its activity. We can have different mutations acting at the same point of the gene. Some of them will be able to induce little changes, if any, in the final expression allowing for a change in the quantitatif final effect (classical homoalleles), but others, acting on the same point could induce a big change in the spatial configuration allowing the production of a different enzyme with or without a functional activity. So the same point of the same gene could produce apparent homoalleles and heteroalleles.
                         
                        Second problem: In the same way I can imagine that mutations acting in different parts of the same gene, could lead to a similar final tridimensional structure of the enzyme, producing just a little change in the quantitatif production of the final effect, as if both mutations were homoallelic, despite that they are acting on different points of the same gene.
                         
                        So, how can we say if two alleles behave as homoalleles or as heteroalleles without genetic studies? Which are the criteria to assume one or the other?
                         
                        Regards
                         
                        Recio
                         
                        From: Recio Joaquin <jrecio99@...>
                        To: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
                        Sent: Friday, August 3, 2012 5:05 PM
                        Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                         
                         
                        Hi Peter,
                         
                        I will take some definitions from an old post of Terry:
                         
                                Homozygous means that the two genes on each of a chromosome pair are the same.
                         
                                Heterozygous means they are each different within the pair
                         
                                Heteroallelic refers to two different mutant alleles and how they relate to each other (not whether they are present together or separate). It implies that they have gene sequence alterations in different functional areas of the gene, so that their effects do not in effect overlap as we see for standard co-dominant alleles.
                         
                                Homoallelic implies that two mutant alleles have alterations in the same functional area of the gene, and therefore behave as differing degrees of the same effect. Virtually all mutant alleles in birds behave in this way. Combine Pallid and Ino and you get an intermediate phenotype. Same happens with Greywing and Clearwing in Budgies, Pastel and NSL Ino in Lovebirds, etc.
                         
                                Parblue mutations have always been the exception in some species and this was initially explained by Peter Bergman using this concept of heteroallelic complementation. In effect it is indicating that the two different alleles have alterations to different functions, which can easily imply they are two different loci.
                         
                                The problem is the use and confusion over the terms heteroallele and homoallele. Stick to heterozygous and homozygous.
                         
                                As for SF parblue, this is a Green bird with one wildtype allele and one parblue allele. Whilst its use persists breeders will continue to think Parblue is dominant and masked by wildtype. To maintain that it doesn't matter because these breeders never mate Parblue x Green is like saying its OK to believe the world is flat because I am never taking a trip out of my country. It is all about a better understanding of the bigger picture, with each fact being an important pre-requisite for further learning. If someone doesn't want to learn, it doesn't matter what terms they use. But then they should not complain that they cannot understand the topic or maintain that they know what they are talking about. Or complain about name changes to mutations for that matter.
                         
                        Considering these definitions the alleles of patched mutations (saphire, indigo, turquoise, ...) should be considered as homoallelic... but when I am treating of patched mutations respective to even mutation I am refering to different genes and not to an heteroallelic relation. I think that this is what Peter was refering to. Isn't it?
                         
                        Anyway, time will tell us.
                         
                        Regards
                         
                        Recio
                         
                        From: Peter Wouters <wouterscalant@...>
                        To: Genetics-Psittacine@yahoogroups.com
                        Sent: Wednesday, August 1, 2012 9:09 PM
                        Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                         
                         
                        Hi Recio,
                         
                        I think you are now reffering to a heteroallelic relation where the different alleles have gene sequence alterations in different functional areas of the gene. Right?
                         
                        Regards
                        Peter
                         
                        Sent: Tuesday, July 31, 2012 4:43 PM
                        Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                         
                         
                        Thank you Madas for your answer. You are extremely smart, as always : Why a mutated bird, with more than 100% of alleles expressivity, does not show a wild phenotype? Why an homozygous Heavy Turquoise does not look like a wild bird? This is the good question I was expecting.
                         
                        The answer to this question is the key point of my reasoning : The homozygous Heavy Turquoise (and any other allele combination showing more than 100% expressivity ... that is: saturating the system) is showing us the wild phenotype of the gene coding for one type of psittacine (the patched psittacine). The lacking psittacine to get the final apparent wild phenotype corresponds to the psittacine produced by the activation of another different gene : the gene coding for the even psittacine. This even psittacin is expressed throughout the whole bird, including the primary flying feathers, and its addition to a saturated patched schema allows to get the final green wild phenotype we all know. This is why we will never get the apparent wild phenotype just by "adding patched partial mutations".
                         
                        As always ... questions before going on ...
                         
                        Regards
                         
                        Recio

                         
                        From: Stefan Adam <mada_s@...>
                        To: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
                        Sent: Tuesday, July 31, 2012 8:03 AM
                        Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                         
                         
                        Hi Recio,
                         
                        interesting thoughts. But there is one mistake within yout theory. If the birds with more then 100% are saturated and showing a wildform phenotype then a homozygous turquoise IRN should have green main flights and green tail. But such a bird is showing blue fligths and tail. See attached pic of Willy which he posted some months (years ;) ) ago. For eyes the "green" wing color is some steps darker then the one of a normal green. I think Willy mentioned it in the past too.
                         
                        Your thougths???
                         
                        S. Adam
                         
                        Von: Recio Joaquin <jrecio99@...>
                        An: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
                        Gesendet: 23:04 Montag, 30.Juli 2012
                        Betreff: [Genetics-Psittacine] Parblues IRN do not exist
                         
                         
                        Hi everybody,
                         
                        I will try to show that parblues IRN do not exist. I will proceed as usually, so everybody will have the time to digest the information.
                         
                        In the last months we have reviewed psittacin type, distribution, intensity, hormonal dependency and age dependent expression trying to find out if there are 1 or 2 genes coding for psittacin production in IRN. Now, after discussion with some of you, I think I also have a genetic reason to think that they are two different genes. Let's go:
                         
                        First basic genetics for better understanding: 
                         
                        The non mutated gene is the wild gene. Every mutation described can be considered as a multiallelic series of at least two alleles : the mutated form and the wild form. These alleles can combine as follows :
                         
                        WildWild .... always wild phenotype
                        MutatedMutated ... always mutated phenotype
                        WildMutated .... the expression depends on the capacity of the Wild gene to produce the final product:
                                1. The mutated gene behaves as recessive .... if just one wild allele is enough to produce 100% of the final product... wild phenotype (Ex: lutino mutation .... split lutino).
                                2. Codominance ...  if one wild allele is able to produce less than100% of the final product and more than 0% ... intermedial phenotype (Ex: dom pied .... SF and DF birds are different).
                                3. The mutated gene behaves as dominant ... if one wild allele is unable to produce any of the final product (0% of final product). The expression of the final product needs the presence of two wild alleles (Ex : grey mutation).
                         
                        So as you can see the situation of recessivity, codominance and dominance depends on the type of wild gene : if just one wild allele activation is able to saturate the system (obtain the final effect) or not. Thus we are not speaking correctly when we say that a mutation "is dominant or recessive", since this characteristic of dominancy or recessivity is not dependent on the mutated gene but it is dependent on the wild gene. We should say that a mutation behaves as dominant or recessive respective to the wild gene.
                         
                        We have just analyzed how the system works considering that the mutated gene is not able at all to activate the system, that is it is an inactive allele. Now we will analyse what happens when the mutated gene is able to partially activate the system to get the final product at a lower percentage than the wild allele (<100%) (this is the case of our "parblues" in IRN).
                         
                        Let's suposse that we have 4 different partial mutations of the wild allele. Let's call them Mut-20, Mut-40, Mut-60 and Mut-80, meaning that each allele is able to partially activate the system at the % numbers expressed. Let's call Mut-0 the mutation unable to activate the system at all (0% of the final product).
                         
                        Let's see which would be the phenotypes of the different combinations whenever one wild gene is able to produce 100% of the final effect (this is the case of the genes coding for psittacin: wild split blue shows green phenotype):
                         
                        WildWild .... 100 + 100 = 200% .... always wild phenotype which is reached at 100% of expression (system saturated)
                         
                        WildMutated: those are call split mutations or heterozygous birds:
                            WildMut-0 .... 100+0 = 100% .... wild phenotype
                            WildMut-20 ..... 100+20 = 120% .... wild phenotype
                            WildMut-40 .... 100+40 = 140% .... wild phenotype
                            WildMut-60 .... 100+60 = 160% .... wild phenotype
                            WildMut-80 ..... 100+80 = 180% .... wild phenotype
                         
                        MutatedMutated : those are the homozygous birds. They can be homoallelic or heteroallelic:
                            Homoallelic :     Mut-0Mut-0 .... 0+0 = 0% activation .... mutated bird ... no expression of the final product.
                                                    Mut-20Mut-20 .... 20+20 = 40% activation .... partial activation at 40%
                                                    Mut-4 0Mut-40 .... 40+40 = 80% activation .... partial activation at 80% 
                                                < /SPAN>    Mut-60Mut-60 .... 60+60 = 120% ..... since saturation is reached at 100% .... wild phenotype
                                              &nb sp;     Mut-80Mut-80 .... 80+80 = 160%  .... again ....  wild phenotype
                            Heteroallelic:     Mut-20Mut-0 .... 20+0 = 20% .... partial activation at 20%
                                                    Mut-20Mut-40 .... 20+40 = 60% .... partial activation at 60%
                                                    Mut-20Mut-60 .... 20+60 = 80% .... partial activation at 80%
                                                    Mut-20Mut-80 ..... 20+80 = 100% .... wild phenotype
                                                    Mut-40Mut-60 ..... 40+60 = 100% .... wild phenotype
                                                    Mut-60Mut-80 ..... 60+80 = 140% ..... wild phenotype
                         
                        As you can see we can get the wild phenotype from partial mutations, without any wild allele in the genetic make up of the birds.
                         
                        For those breeding IRN you can change Mut-0 by Blue, Mut-20 by Saphire, Mut-40 by Indigo, Mut-60 by Light Turquoise and Mut-80 by Heavy Turquoise, but this does not mean that the mutations identified by these morphotypes are the only partial mutations in IRN (we could have a Mut-5, Mut-15, Mut 33, ....).
                         
                        Time for questions before going further.
                         
                        Regards
                         
                        Recio
                         








                      • Recio Joaquin
                        Hi Deon,   I adept completely to the phylosophical part (even and specially to the criteria of begining of life) ... but this forum is about a different
                        Message 11 of 27 , Aug 4 11:54 AM
                          Hi Deon,
                           
                          I adept completely to the phylosophical part (even and specially to the criteria of begining of life) ... but this forum is about a different subject.
                           
                          A homozygotic parblue can never be phenotypically wild-type. Are you sure? Remember what you have just written : We live in a changing world and so we have to adapt and start thinking about the inadequacies of established systems and start formulating new criteria and new directions of thinking, considering what we know today and what we believe we know.
                          I think that it depends whether this parblue acts through an inhibitory mechanism (then you would be rigth) or through an activatory mechanism (then your sentence would not be correct). Imagine a parblue mutation able to decrease the final psittacine of 40% (it means that 60% of the psittacine is expressed) when only one allele of this parblue is expressed (Ex ParblueBlue).
                           
                          1. If activatory mechanism :
                          WildParblue ..... wild phenotype
                          ParblueBlue ..... parblue phenotype (psittacine expression of 60% since there is only an activation of 60% of the system leading to psittacin production)
                          ParblueParblue ..... wild phenotype since the theoretical capacity of psittacine production is 120% (60% from each Parblue allele) .... wild phenotype.
                           
                          2. If inhibitory mechanism:
                          WildParblue ..... wild phenotype.
                          ParblueBlue ..... parblue phenotype (psittacine expression of 60% since there is a block of 40% in the capacity of the metabolic path leading to psittacin production due to the increase in the production of an inhibitory agent).
                          ParblueParblue ..... parblue phenotype expressing only 20%. The homozygous form of the Parblue only expresses 20% since each Parblue allele blocks 40% of the expression. This is a bluish phenotype.
                           
                          So, for a Parblue mutation able to express more than 50% of the final product when it is present in the heterozygous form (BlueParblue) and acting through an activatory mechanism, it would be posible to get an apparent wild phenotype in the homozygous form (ParblueParblue). Please, if you think that I am wrong .... could you tell me specifically why/where in my reasoning?
                           
                          Why everybody accepts the same reasoning for an activatory mechanism if the parblue mutation expresses less than 50% of the final product (let's say 30%) in the heterozygous form, so that in the homozygous form (60% of psittacin expression) we get a greener bird with less than 100% expression, that is a heavy parblue? Is this reasoning valid only when it conforts our previous ideas? Let's open our minds ... and if I am wrong ... let me know it .... with reasons.
                           
                          Maybe the problem is that you are thinking that the mutated genes are the same for both mechanisms ... but this is wrong : only in the activatory mechanism we can properly speak of parblues because the partially mutated gene is the same which completely blocks psittacin production (Blue). In the inhibitory mechanism the mutated gene is different. It is coding for a different enzyme, acting by an inhibitory mechanism in psittacine synthesis ... and this is the reason that I said that we can not compare two apparent parblues mutations in different species when the homozygous parblues behave differently (greener in one specie and bluer in the other).
                           
                          Even with 80% psittacin retention in a homoallelic homozygous event, there is still a 20% loss of...exactly what? Quantitative decrease of psittacins as a collective homogenous mass of different psittacins? What about the quality, where are the control points for facets of psittacins; colour tone, brilliance, hue, interactions, all the possible modifications, the millions of available colour expressions.
                           
                          I agree ... and this is why we are here.... trying to approach the "truth", even that our models are too simple. Knowledge is like a sphere : when it increases, the number of external points touching the "unknown" also increase, and this is why the most knowledgable people are those with more doubts and questions. I am sure that some of the persons who doubt the most here are Terry and Inte ... and that this is the reason their presence is rare : we can not answer their questions ... but our questions could trigger new ideas in their minds, so they both should be a little more presents.
                           
                          Regards
                           
                          Recio
                          From: Deon Smith <gms1@...>
                          To: Genetics Psittacine <genetics-psittacine@yahoogroups.com>
                          Sent: Saturday, August 4, 2012 2:51 PM
                          Subject: Fw: [Genetics-Psittacine] Parblues IRN do not exist

                           
                          Sorry, correction
                           
                          Sent: Saturday, August 04, 2012 2:34 PM
                          Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                           
                           
                          We are trying to align natural events within boundaries/divisions we have created, instead of the other way round. This all in an effort to understand things according to present knowledge.
                          What we have seen lately, is the fading of man-made boundaries in established man-made classification systems with the advances in and release of knowledge. As an example, look at the definitions for inheritance behaviour; dominant, recessive etc. We live in a changing world and so we have to adapt and start thinking about the inadequacies of established systems and start formulating new criteria and new directions of thinking, considering what we know today and what we believe we know.
                           
                          Look at the man-made divisions in the development of a new life in legal definitions of when a developing new individual may be executed through legal abortion, decided on by Someone playing God that is putting up divisions in a process of programmed continuing development.
                           
                          A homozygotic parblue can never be phenotypically wild-type. Even with 80% psittacin retention in a homoallelic homozygous event, there is still a 20% loss of...exactly what? Quantitative decrease of psittacins as a collective homogenous mass of different psittacins? What about the quality, where are the control points for facets of psittacins; colour tone, brilliance, hue, interactions, all the possible modifications, the millions of available colour expressions. The exchange of one metal molecule for another in the white paper for colour production, brought about by a single base substitution and the major effect of such a minute alteration.
                           
                          Deon
                           
                          Sent: Saturday, August 04, 2012 12:52 PM
                          Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                           
                           
                          Peter, Deon, Terry, Wynand, .... every other with knowledge in "the smart stuff",
                           
                          I have checked that the definitions of homoalleles and heteroalleles made by Terry are correct... but I have a problem for understanding it : it seems that the changes in nucleotide composition in one specific part of a gene will always produce a change in the quantity of the RNAm produced ... a change in the quantity of the protein produced ... a quantitatif change in the final effect we see .... but changes in a different part of the same gene will finally produce,  by a similar mechanisms, quantitatif changes in a different final effect that we see. In fact it seems that those heteroalleles act as if they were consecutive genes, but, I guess, without a stop codon. Is it the case? If it is the case ... how can we make the difference between two extremely linked genes and two heteroalleles? ... and which would be the functional differences allowing for identification of one or another?
                           
                          First problem : most of the proteins involved in colour regulation are enzymes. The activity of enzymes is highly dependent on its tridimensional structure, and this structure depends mainly on the disposition of some specific aminoacids (those showing an asymetric -NH3 or -COOH), hydrogen bridges, ... that is, on the repartition of electric charges. A change in just one aminoacid can completely change the tridimensional structure of the enzyme and, thus, its activity. We can have different mutations acting at the same point of the gene. Some of them will be able to induce little changes, if any, in the final expression allowing for a change in the quantitatif final effect (classical homoalleles), but others, acting on the same point could induce a big change in the spatial configuration allowing the production of a different enzyme with or without a functional activity. So the same point of the same gene could produce apparent homoalleles and heteroalleles.
                           
                          Second problem: In the same way I can imagine that mutations acting in different parts of the same gene, could lead to a similar final tridimensional structure of the enzyme, producing just a little change in the quantitatif production of the final effect, as if both mutations were homoallelic, despite that they are acting on different points of the same gene.
                           
                          So, how can we say if two alleles behave as homoalleles or as heteroalleles without genetic studies? Which are the criteria to assume one or the other?
                           
                          Regards
                           
                          Recio
                           


                        • Deon Smith
                          To get back to basics: a gene is a functional unit of heredity. It is a segment of DNA that is responsible for the physical and inheritable characteristics or
                          Message 12 of 27 , Aug 4 3:40 PM
                            To get back to basics: a gene is a functional unit of heredity. It is a segment of DNA that is responsible for the physical and inheritable characteristics or phenotype of a living organism. A gene is made up of sequences of base pairs of variable length, where each base pair may potentially be subject to mutation; each base pair being physically able to have 3 different alleles of forms, apart from the wild type allele. But a gene may span many many base pairs. Your quotation of Terry’s definition and Peter’s interpretation is spot on, but the crucial word is functional. When we get to functional units we have to address exons and introns which I will  not go into now, suffice to say that a functional unit of a gene codes for specific proteins and enzymes, which may be changed by different modifiers and mutations.
                            Due to the complexity of gene structure, different segments of a gene may mutate, giving origin to different alleles which may appear (act) like another gene, in which case we talk of heteroalleles. When the same functional unit is involved, we get homoallelic relations.
                             
                            The control of psittacins in toto must be a massive task for one or two genes, with very little research results available on commercially-directed studies on poultry as an example. We must assume that more than one gene, or many, may be involved, given the complexity of psittacin production that must be in place, and that these genes may be massive in size, with many functional segments but still forming part on a specified gene. Read the first sentence again.
                             
                            If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele? How will this then be proven?
                             
                            I believe that the expression of the normal wildtype allele is the normal state and not an additional expense of energy, therefore mutations at these loci are inhibitory in nature and the homozygote appears closer to the normal wildtype phenotype, unless we have a situation where the homozygotic form appears closer to the complete mutation than the heterozygote, that we see in other spp. But in this latter instance we must not overlook epistasis in the heterozygote, where one gene could code for a protein preventing transcription of the other gene. Also, epistasis must be differentiated from dominance at the homoallelic level that points to an interaction between alleles at the same gene functional unit. And not the least, intragenic complementation but this must refer to heteroalleles which is not applicable here, it refers to two alleles complementing in the heteroallelic event; we are referring to a homoallelic difference, unless we have an unexpected situation of heteroalleles, other than in the ringneck. These 3 functional options may all explain the phenomenon where the homozygote appears closer to the complete mutation allele than the heterozygote.
                             
                            Deon
                             
                             
                             
                             
                             
                             
                            Sent: Saturday, August 04, 2012 8:54 PM
                            Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                             
                             

                            Hi Deon,
                             
                            I adept completely to the phylosophical part (even and specially to the criteria of begining of life) ... but this forum is about a different subject.
                             
                            A homozygotic parblue can never be phenotypically wild-type. Are you sure? Remember what you have just written : We live in a changing world and so we have to adapt and start thinking about the inadequacies of established systems and start formulating new criteria and new directions of thinking, considering what we know today and what we believe we know.
                            I think that it depends whether this parblue acts through an inhibitory mechanism (then you would be rigth) or through an activatory mechanism (then your sentence would not be correct). Imagine a parblue mutation able to decrease the final psittacine of 40% (it means that 60% of the psittacine is expressed) when only one allele of this parblue is expressed (Ex ParblueBlue).
                             
                            1. If activatory mechanism :
                            WildParblue ..... wild phenotype
                            ParblueBlue ..... parblue phenotype (psittacine expression of 60% since there is only an activation of 60% of the system leading to psittacin production)
                            ParblueParblue ..... wild phenotype since the theoretical capacity of psittacine production is 120% (60% from each Parblue allele) .... wild phenotype.
                             
                            2. If inhibitory mechanism:
                            WildParblue ..... wild phenotype.
                            ParblueBlue ..... parblue phenotype (psittacine expression of 60% since there is a block of 40% in the capacity of the metabolic path leading to psittacin production due to the increase in the production of an inhibitory agent).
                            ParblueParblue ..... parblue phenotype expressing only 20%. The homozygous form of the Parblue only expresses 20% since each Parblue allele blocks 40% of the expression. This is a bluish phenotype.
                             
                            So, for a Parblue mutation able to express more than 50% of the final product when it is present in the heterozygous form (BlueParblue) and acting through an activatory mechanism, it would be posible to get an apparent wild phenotype in the homozygous form (ParblueParblue). Please, if you think that I am wrong .... could you tell me specifically why/where in my reasoning?
                             
                            Why everybody accepts the same reasoning for an activatory mechanism if the parblue mutation expresses less than 50% of the final product (let's say 30%) in the heterozygous form, so that in the homozygous form (60% of psittacin expression) we get a greener bird with less than 100% expression, that is a heavy parblue? Is this reasoning valid only when it conforts our previous ideas? Let's open our minds ... and if I am wrong ... let me know it .... with reasons.
                             
                            Maybe the problem is that you are thinking that the mutated genes are the same for both mechanisms ... but this is wrong : only in the activatory mechanism we can properly speak of parblues because the partially mutated gene is the same which completely blocks psittacin production (Blue). In the inhibitory mechanism the mutated gene is different. It is coding for a different enzyme, acting by an inhibitory mechanism in psittacine synthesis ... and this is the reason that I said that we can not compare two apparent parblues mutations in different species when the homozygous parblues behave differently (greener in one specie and bluer in the other).
                             
                            Even with 80% psittacin retention in a homoallelic homozygous event, there is still a 20% loss of...exactly what? Quantitative decrease of psittacins as a collective homogenous mass of different psittacins? What about the quality, where are the control points for facets of psittacins; colour tone, brilliance, hue, interactions, all the possible modifications, the millions of available colour expressions.
                             
                            I agree ... and this is why we are here.... trying to approach the "truth", even that our models are too simple. Knowledge is like a sphere : when it increases, the number of external points touching the "unknown" also increase, and this is why the most knowledgable people are those with more doubts and questions. I am sure that some of the persons who doubt the most here are Terry and Inte ... and that this is the reason their presence is rare : we can not answer their questions ... but our questions could trigger new ideas in their minds, so they both should be a little more presents.
                             
                            Regards
                             
                            Recio
                            From: Deon Smith <gms1@...>
                            To: Genetics Psittacine <genetics-psittacine@yahoogroups.com>
                            Sent: Saturday, August 4, 2012 2:51 PM
                            Subject: Fw: [Genetics-Psittacine] Parblues IRN do not exist
                             
                             
                            Sorry, correction
                             
                            Sent: Saturday, August 04, 2012 2:34 PM
                            Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                             
                             
                            We are trying to align natural events within boundaries/divisions we have created, instead of the other way round. This all in an effort to understand things according to present knowledge.
                            What we have seen lately, is the fading of man-made boundaries in established man-made classification systems with the advances in and release of knowledge. As an example, look at the definitions for inheritance behaviour; dominant, recessive etc. We live in a changing world and so we have to adapt and start thinking about the inadequacies of established systems and start formulating new criteria and new directions of thinking, considering what we know today and what we believe we know.
                             
                            Look at the man-made divisions in the development of a new life in legal definitions of when a developing new individual may be executed through legal abortion, decided on by Someone playing God that is putting up divisions in a process of programmed continuing development.
                             
                            A homozygotic parblue can never be phenotypically wild-type. Even with 80% psittacin retention in a homoallelic homozygous event, there is still a 20% loss of...exactly what? Quantitative decrease of psittacins as a collective homogenous mass of different psittacins? What about the quality, where are the control points for facets of psittacins; colour tone, brilliance, hue, interactions, all the possible modifications, the millions of available colour expressions. The exchange of one metal molecule for another in the white paper for colour production, brought about by a single base substitution and the major effect of such a minute alteration.
                             
                            Deon
                             
                            Sent: Saturday, August 04, 2012 12:52 PM
                            Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                             
                             
                            Peter, Deon, Terry, Wynand, .... every other with knowledge in "the smart stuff",
                             
                            I have checked that the definitions of homoalleles and heteroalleles made by Terry are correct... but I have a problem for understanding it : it seems that the changes in nucleotide composition in one specific part of a gene will always produce a change in the quantity of the RNAm produced ... a change in the quantity of the protein produced ... a quantitatif change in the final effect we see .... but changes in a different part of the same gene will finally produce,  by a similar mechanisms, quantitatif changes in a different final effect that we see. In fact it seems that those heteroalleles act as if they were consecutive genes, but, I guess, without a stop codon. Is it the case? If it is the case ... how can we make the difference between two extremely linked genes and two heteroalleles? ... and which would be the functional differences allowing for identification of one or another?
                             
                            First problem : most of the proteins involved in colour regulation are enzymes. The activity of enzymes is highly dependent on its tridimensional structure, and this structure depends mainly on the disposition of some specific aminoacids (those showing an asymetric -NH3 or -COOH), hydrogen bridges, ... that is, on the repartition of electric charges. A change in just one aminoacid can completely change the tridimensional structure of the enzyme and, thus, its activity. We can have different mutations acting at the same point of the gene. Some of them will be able to induce little changes, if any, in the final expression allowing for a change in the quantitatif final effect (classical homoalleles), but others, acting on the same point could induce a big change in the spatial configuration allowing the production of a different enzyme with or without a functional activity. So the same point of the same gene could produce apparent homoalleles and heteroalleles.
                             
                            Second problem: In the same way I can imagine that mutations acting in different parts of the same gene, could lead to a similar final tridimensional structure of the enzyme, producing just a little change in the quantitatif production of the final effect, as if both mutations were homoallelic, despite that they are acting on different points of the same gene.
                             
                            So, how can we say if two alleles behave as homoalleles or as heteroalleles without genetic studies? Which are the criteria to assume one or the other?
                             
                            Regards
                             
                            Recio
                             


                          • Recio Joaquin
                            Hi Deon,   You have explained some of the possibilities to explain results at the genetic level. You could even add transformations of the initially produced
                            Message 13 of 27 , Aug 5 5:29 AM
                              Hi Deon,
                               
                              You have explained some of the possibilities to explain results at the genetic level. You could even add transformations of the initially produced protein so that it is sliced in different proteins with different functions, even that they come all of them from the same gene (Ex: proopiomelanocortin producing several hormones and peptides : http://en.wikipedia.org/wiki/Proopiomelanocortin) ... but the question remains intact :
                               
                              If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele?
                               
                              I will tell you a history so you will understand that wild alleles do not "exist" (as well as mutated alleles) :
                              Recio was a selfconfident man leaving in Whiteland. In Whiteland every animal was white because of the white environement due to snow : there were white rabbits, white mice, .... and wild IRNs with a white phenotype and black eyes who had wonderfully adapted to the environement centuries ago. From men memory these birds had always been there, and they were even represented in the oldest totems that archeologist have found. Recio detected that from time to time there were spontanous mutations in the white wild IRN producing strange birds who were called dom pied IRN, since the mutation acted as dominant and the birds showed a patched expression of melanin. Some bird breeders in Whiteland had even proven that whenever two heterozygous birds were paired, they could get a strange mutant showing a green phenotype. Thus the homozygous form of the dom pied mutation was called green mutant.
                              At the time the first green mutant was detected Recio contacted his friend Deon who was living in a warm country and was also a bird hobby man. He sent to him some pics of the wild bird (white phenotype), the heterozygous bird (dom pied) and the homozygous bird (green mutant) telling to Deon that this strange mutation behaves as incomplete dominant. When Deon received the pics with the labelled mutations, he was sure that Recio had made a mistake when labeling the pics, because in his country the wild bird was green and the homozygous mutation was white.
                               
                              Tell me my friends ... who of both Recio or Deon was right? Were both right? This is my feeling .... and if both of them were right it means that the concept of wild allele should be changed by the concept of "prevalent" allele in a given population. If the different alleles of a gene are considered in a "democratic" way, with all of them having the same "importance", we will accpet easierly that what can happen to one of them, can happen to any other. Thus our initial question ....
                               
                              If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele?
                               
                              .... could be reformuleted as follows:
                               
                              If a homozygous homoallelic event appears phenotypically identical to the mutant type, does it represent an allele at all, different to the mutant-type allele?
                               
                              We have changed wild by mutant (which in fact is the same as we have seen) and now it seems easier to reformulate the question as : could we get the same phenotypic expression from two different homozygous mutant alleles?
                               
                              What's you feeling?
                               
                              Recio

                              From: Deon Smith <gms1@...>
                              To: Genetics-Psittacine@yahoogroups.com
                              Sent: Sunday, August 5, 2012 12:40 AM
                              Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist

                               
                              To get back to basics: a gene is a functional unit of heredity. It is a segment of DNA that is responsible for the physical and inheritable characteristics or phenotype of a living organism.A gene is made up of sequences of base pairs of variable length, where each base pair may potentially be subject to mutation; each base pair being physically able to have 3 different alleles of forms, apart from the wild type allele. But a gene may span many many base pairs. Your quotation of Terry’s definition and Peter’s interpretation is spot on, but the crucial word is functional. When we get to functional units we have to address exons and introns which I will  not go into now, suffice to say that a functional unit of a gene codes for specific proteins and enzymes, which may be changed by different modifiers and mutations.
                              Due to the complexity of gene structure, different segments of a gene may mutate, giving origin to different alleles which may appear (act) like another gene, in which case we talk of heteroalleles. When the same functional unit is involved, we get homoallelic relations.
                               
                              The control of psittacins in toto must be a massive task for one or two genes, with very little research results available on commercially-directed studies on poultry as an example. We must assume that more than one gene, or many, may be involved, given the complexity of psittacin production that must be in place, and that these genes may be massive in size, with many functional segments but still forming part on a specified gene. Read the first sentence again.
                               
                              If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele? How will this then be proven?
                               
                              I believe that the expression of the normal wildtype allele is the normal state and not an additional expense of energy, therefore mutations at these loci are inhibitory in nature and the homozygote appears closer to the normal wildtype phenotype, unless we have a situation where the homozygotic form appears closer to the complete mutation than the heterozygote, that we see in other spp. But in this latter instance we must not overlook epistasis in the heterozygote, where one gene could code for a protein preventing transcription of the other gene. Also, epistasis must be differentiated from dominance at the homoallelic level that points to an interaction between alleles at the same gene functional unit. And not the least, intragenic complementation but this must refer to heteroalleles which is not applicable here, it refers to two alleles complementing in the heteroallelic event; we are referring to a homoallelic difference, unless we have an unexpected situation of heteroalleles, other than in the ringneck. These 3 functional options may all explain the phenomenon where the homozygote appears closer to the complete mutation allele than the heterozygote.
                               
                              Deon
                               
                               
                               
                               
                               
                               
                              Sent: Saturday, August 04, 2012 8:54 PM
                              Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                               
                               
                              Hi Deon,
                               
                              I adept completely to the phylosophical part (even and specially to the criteria of begining of life) ... but this forum is about a different subject.
                               
                              A homozygotic parblue can never be phenotypically wild-type. Are you sure? Remember what you have just written : We live in a changing world and so we have to adapt and start thinking about the inadequacies of established systems and start formulating new criteria and new directions of thinking, considering what we know today and what we believe we know.
                              I think that it depends whether this parblue acts through an inhibitory mechanism (then you would be rigth) or through an activatory mechanism (then your sentence would not be correct). Imagine a parblue mutation able to decrease the final psittacine of 40% (it means that 60% of the psittacine is expressed) when only one allele of this parblue is expressed (Ex ParblueBlue).
                               
                              1. If activatory mechanism :
                              WildParblue ..... wild phenotype
                              ParblueBlue ..... parblue phenotype (psittacine expression of 60% since there is only an activation of 60% of the system leading to psittacin production)
                              ParblueParblue ..... wild phenotype since the theoretical capacity of psittacine production is 120% (60% from each Parblue allele) .... wild phenotype.
                               
                              2. If inhibitory mechanism:
                              WildParblue ..... wild phenotype.
                              ParblueBlue ..... parblue phenotype (psittacine expression of 60% since there is a block of 40% in the capacity of the metabolic path leading to psittacin production due to the increase in the production of an inhibitory agent).
                              ParblueParblue ..... parblue phenotype expressing only 20%. The homozygous form of the Parblue only expresses 20% since each Parblue allele blocks 40% of the expression. This is a bluish phenotype.
                               
                              So, for a Parblue mutation able to express more than 50% of the final product when it is present in the heterozygous form (BlueParblue) and acting through an activatory mechanism, it would be posible to get an apparent wild phenotype in the homozygous form (ParblueParblue). Please, if you think that I am wrong .... could you tell me specifically why/where in my reasoning?
                               
                              Why everybody accepts the same reasoning for an activatory mechanism if the parblue mutation expresses less than 50% of the final product (let's say 30%) in the heterozygous form, so that in the homozygous form (60% of psittacin expression) we get a greener bird with less than 100% expression, that is a heavy parblue? Is this reasoning valid only when it conforts our previous ideas? Let's open our minds ... and if I am wrong ... let me know it .... with reasons.
                               
                              Maybe the problem is that you are thinking that the mutated genes are the same for both mechanisms ... but this is wrong : only in the activatory mechanism we can properly speak of parblues because the partially mutated gene is the same which completely blocks psittacin production (Blue). In the inhibitory mechanism the mutated gene is different. It is coding for a different enzyme, acting by an inhibitory mechanism in psittacine synthesis ... and this is the reason that I said that we can not compare two apparent parblues mutations in different species when the homozygous parblues behave differently (greener in one specie and bluer in the other).
                               
                              Even with 80% psittacin retention in a homoallelic homozygous event, there is still a 20% loss of...exactly what? Quantitative decrease of psittacins as a collective homogenous mass of different psittacins? What about the quality, where are the control points for facets of psittacins; colour tone, brilliance, hue, interactions, all the possible modifications, the millions of available colour expressions.
                               
                              I agree ... and this is why we are here.... trying to approach the "truth", even that our models are too simple. Knowledge is like a sphere : when it increases, the number of external points touching the "unknown" also increase, and this is why the most knowledgable people are those with more doubts and questions. I am sure that some of the persons who doubt the most here are Terry and Inte ... and that this is the reason their presence is rare : we can not answer their questions ... but our questions could trigger new ideas in their minds, so they both should be a little more presents.
                               
                              Regards
                               
                              Recio
                              From: Deon Smith <gms1@...>
                              To: Genetics Psittacine <genetics-psittacine@yahoogroups.com>
                              Sent: Saturday, August 4, 2012 2:51 PM
                              Subject: Fw: [Genetics-Psittacine] Parblues IRN do not exist
                               
                               
                              Sorry, correction
                               
                              Sent: Saturday, August 04, 2012 2:34 PM
                              Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                               
                               
                              We are trying to align natural events within boundaries/divisions we have created, instead of the other way round. This all in an effort to understand things according to present knowledge.
                              What we have seen lately, is the fading of man-made boundaries in established man-made classification systems with the advances in and release of knowledge. As an example, look at the definitions for inheritance behaviour; dominant, recessive etc. We live in a changing world and so we have to adapt and start thinking about the inadequacies of established systems and start formulating new criteria and new directions of thinking, considering what we know today and what we believe we know.
                               
                              Look at the man-made divisions in the development of a new life in legal definitions of when a developing new individual may be executed through legal abortion, decided on by Someone playing God that is putting up divisions in a process of programmed continuing development.
                               
                              A homozygotic parblue can never be phenotypically wild-type. Even with 80% psittacin retention in a homoallelic homozygous event, there is still a 20% loss of...exactly what? Quantitative decrease of psittacins as a collective homogenous mass of different psittacins? What about the quality, where are the control points for facets of psittacins; colour tone, brilliance, hue, interactions, all the possible modifications, the millions of available colour expressions. The exchange of one metal molecule for another in the white paper for colour production, brought about by a single base substitution and the major effect of such a minute alteration.
                               
                              Deon
                               
                              Sent: Saturday, August 04, 2012 12:52 PM
                              Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                               
                               
                              Peter, Deon, Terry, Wynand, .... every other with knowledge in "the smart stuff",
                               
                              I have checked that the definitions of homoalleles and heteroalleles made by Terry are correct... but I have a problem for understanding it : it seems that the changes in nucleotide composition in one specific part of a gene will always produce a change in the quantity of the RNAm produced ... a change in the quantity of the protein produced ... a quantitatif change in the final effect we see .... but changes in a different part of the same gene will finally produce,  by a similar mechanisms, quantitatif changes in a different final effect that we see. In fact it seems that those heteroalleles act as if they were consecutive genes, but, I guess, without a stop codon. Is it the case? If it is the case ... how can we make the difference between two extremely linked genes and two heteroalleles? ... and which would be the functional differences allowing for identification of one or another?
                               
                              First problem : most of the proteins involved in colour regulation are enzymes. The activity of enzymes is highly dependent on its tridimensional structure, and this structure depends mainly on the disposition of some specific aminoacids (those showing an asymetric -NH3 or -COOH), hydrogen bridges, ... that is, on the repartition of electric charges. A change in just one aminoacid can completely change the tridimensional structure of the enzyme and, thus, its activity. We can have different mutations acting at the same point of the gene. Some of them will be able to induce little changes, if any, in the final expression allowing for a change in the quantitatif final effect (classical homoalleles), but others, acting on the same point could induce a big change in the spatial configuration allowing the production of a different enzyme with or without a functional activity. So the same point of the same gene could produce apparent homoalleles and heteroalleles.
                               
                              Second problem: In the same way I can imagine that mutations acting in different parts of the same gene, could lead to a similar final tridimensional structure of the enzyme, producing just a little change in the quantitatif production of the final effect, as if both mutations were homoallelic, despite that they are acting on different points of the same gene.
                               
                              So, how can we say if two alleles behave as homoalleles or as heteroalleles without genetic studies? Which are the criteria to assume one or the other?
                               
                              Regards
                               
                              Recio
                               




                            • Recio Joaquin
                              One correction : the green mutant in Whiteland was not green but blue ... but I am sure you have all understand what I was meaning with that tale.   Recio
                              Message 14 of 27 , Aug 5 6:07 AM
                                One correction : the green mutant in Whiteland was not green but blue ... but I am sure you have all understand what I was meaning with that tale.
                                 
                                Recio

                                From: Recio Joaquin <jrecio99@...>
                                To: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
                                Sent: Sunday, August 5, 2012 2:29 PM
                                Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist

                                 
                                Hi Deon,
                                 
                                You have explained some of the possibilities to explain results at the genetic level. You could even add transformations of the initially produced protein so that it is sliced in different proteins with different functions, even that they come all of them from the same gene (Ex: proopiomelanocortin producing several hormones and peptides : http://en.wikipedia.org/wiki/Proopiomelanocortin) ... but the question remains intact :
                                 
                                If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele?
                                 
                                I will tell you a history so you will understand that wild alleles do not "exist" (as well as mutated alleles) :
                                Recio was a selfconfident man leaving in Whiteland. In Whiteland every animal was white because of the white environement due to snow : there were white rabbits, white mice, .... and wild IRNs with a white phenotype and black eyes who had wonderfully adapted to the environement centuries ago. From men memory these birds had always been there, and they were even represented in the oldest totems that archeologist have found. Recio detected that from time to time there were spontanous mutations in the white wild IRN producing strange birds who were called dom pied IRN, since the mutation acted as dominant and the birds showed a patched expression of melanin. Some bird breeders in Whiteland had even proven that whenever two heterozygous birds were paired, they could get a strange mutant showing a green phenotype. Thus the homozygous form of the dom pied mutation was called green mutant.
                                At the time the first green mutant was detected Recio contacted his friend Deon who was living in a warm country and was also a bird hobby man. He sent to him some pics of the wild bird (white phenotype), the heterozygous bird (dom pied) and the homozygous bird (green mutant) telling to Deon that this strange mutation behaves as incomplete dominant. When Deon received the pics with the labelled mutations, he was sure that Recio had made a mistake when labeling the pics, because in his country the wild bird was green and the homozygous mutation was white.
                                 
                                Tell me my friends ... who of both Recio or Deon was right? Were both right? This is my feeling .... and if both of them were right it means that the concept of wild allele should be changed by the concept of "prevalent" allele in a given population. If the different alleles of a gene are considered in a "democratic" way, with all of them having the same "importance", we will accpet easierly that what can happen to one of them, can happen to any other. Thus our initial question ....
                                 
                                If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele?
                                 
                                .... could be reformuleted as follows:
                                 
                                If a homozygous homoallelic event appears phenotypically identical to the mutant type, does it represent an allele at all, different to the mutant-type allele?
                                 
                                We have changed wild by mutant (which in fact is the same as we have seen) and now it seems easier to reformulate the question as : could we get the same phenotypic expression from two different homozygous mutant alleles?
                                 
                                What's you feeling?
                                 
                                Recio

                                From: Deon Smith <gms1@...>
                                To: Genetics-Psittacine@yahoogroups.com
                                Sent: Sunday, August 5, 2012 12:40 AM
                                Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist

                                 
                                To get back to basics: a gene is a functional unit of heredity. It is a segment of DNA that is responsible for the physical and inheritable characteristics or phenotype of a living organism.A gene is made up of sequences of base pairs of variable length, where each base pair may potentially be subject to mutation; each base pair being physically able to have 3 different alleles of forms, apart from the wild type allele. But a gene may span many many base pairs. Your quotation of Terry’s definition and Peter’s interpretation is spot on, but the crucial word is functional. When we get to functional units we have to address exons and introns which I will  not go into now, suffice to say that a functional unit of a gene codes for specific proteins and enzymes, which may be changed by different modifiers and mutations.
                                Due to the complexity of gene structure, different segments of a gene may mutate, giving origin to different alleles which may appear (act) like another gene, in which case we talk of heteroalleles. When the same functional unit is involved, we get homoallelic relations.
                                 
                                The control of psittacins in toto must be a massive task for one or two genes, with very little research results available on commercially-directed studies on poultry as an example. We must assume that more than one gene, or many, may be involved, given the complexity of psittacin production that must be in place, and that these genes may be massive in size, with many functional segments but still forming part on a specified gene. Read the first sentence again.
                                 
                                If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele? How will this then be proven?
                                 
                                I believe that the expression of the normal wildtype allele is the normal state and not an additional expense of energy, therefore mutations at these loci are inhibitory in nature and the homozygote appears closer to the normal wildtype phenotype, unless we have a situation where the homozygotic form appears closer to the complete mutation than the heterozygote, that we see in other spp. But in this latter instance we must not overlook epistasis in the heterozygote, where one gene could code for a protein preventing transcription of the other gene. Also, epistasis must be differentiated from dominance at the homoallelic level that points to an interaction between alleles at the same gene functional unit. And not the least, intragenic complementation but this must refer to heteroalleles which is not applicable here, it refers to two alleles complementing in the heteroallelic event; we are referring to a homoallelic difference, unless we have an unexpected situation of heteroalleles, other than in the ringneck. These 3 functional options may all explain the phenomenon where the homozygote appears closer to the complete mutation allele than the heterozygote.
                                 
                                Deon
                                 
                                 
                                 
                                 
                                 
                                 
                                Sent: Saturday, August 04, 2012 8:54 PM
                                Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                 
                                 
                                Hi Deon,
                                 
                                I adept completely to the phylosophical part (even and specially to the criteria of begining of life) ... but this forum is about a different subject.
                                 
                                A homozygotic parblue can never be phenotypically wild-type. Are you sure? Remember what you have just written : We live in a changing world and so we have to adapt and start thinking about the inadequacies of established systems and start formulating new criteria and new directions of thinking, considering what we know today and what we believe we know.
                                I think that it depends whether this parblue acts through an inhibitory mechanism (then you would be rigth) or through an activatory mechanism (then your sentence would not be correct). Imagine a parblue mutation able to decrease the final psittacine of 40% (it means that 60% of the psittacine is expressed) when only one allele of this parblue is expressed (Ex ParblueBlue).
                                 
                                1. If activatory mechanism :
                                WildParblue ..... wild phenotype
                                ParblueBlue ..... parblue phenotype (psittacine expression of 60% since there is only an activation of 60% of the system leading to psittacin production)
                                ParblueParblue ..... wild phenotype since the theoretical capacity of psittacine production is 120% (60% from each Parblue allele) .... wild phenotype.
                                 
                                2. If inhibitory mechanism:
                                WildParblue ..... wild phenotype.
                                ParblueBlue ..... parblue phenotype (psittacine expression of 60% since there is a block of 40% in the capacity of the metabolic path leading to psittacin production due to the increase in the production of an inhibitory agent).
                                ParblueParblue ..... parblue phenotype expressing only 20%. The homozygous form of the Parblue only expresses 20% since each Parblue allele blocks 40% of the expression. This is a bluish phenotype.
                                 
                                So, for a Parblue mutation able to express more than 50% of the final product when it is present in the heterozygous form (BlueParblue) and acting through an activatory mechanism, it would be posible to get an apparent wild phenotype in the homozygous form (ParblueParblue). Please, if you think that I am wrong .... could you tell me specifically why/where in my reasoning?
                                 
                                Why everybody accepts the same reasoning for an activatory mechanism if the parblue mutation expresses less than 50% of the final product (let's say 30%) in the heterozygous form, so that in the homozygous form (60% of psittacin expression) we get a greener bird with less than 100% expression, that is a heavy parblue? Is this reasoning valid only when it conforts our previous ideas? Let's open our minds ... and if I am wrong ... let me know it .... with reasons.
                                 
                                Maybe the problem is that you are thinking that the mutated genes are the same for both mechanisms ... but this is wrong : only in the activatory mechanism we can properly speak of parblues because the partially mutated gene is the same which completely blocks psittacin production (Blue). In the inhibitory mechanism the mutated gene is different. It is coding for a different enzyme, acting by an inhibitory mechanism in psittacine synthesis ... and this is the reason that I said that we can not compare two apparent parblues mutations in different species when the homozygous parblues behave differently (greener in one specie and bluer in the other).
                                 
                                Even with 80% psittacin retention in a homoallelic homozygous event, there is still a 20% loss of...exactly what? Quantitative decrease of psittacins as a collective homogenous mass of different psittacins? What about the quality, where are the control points for facets of psittacins; colour tone, brilliance, hue, interactions, all the possible modifications, the millions of available colour expressions.
                                 
                                I agree ... and this is why we are here.... trying to approach the "truth", even that our models are too simple. Knowledge is like a sphere : when it increases, the number of external points touching the "unknown" also increase, and this is why the most knowledgable people are those with more doubts and questions. I am sure that some of the persons who doubt the most here are Terry and Inte ... and that this is the reason their presence is rare : we can not answer their questions ... but our questions could trigger new ideas in their minds, so they both should be a little more presents.
                                 
                                Regards
                                 
                                Recio
                                From: Deon Smith <gms1@...>
                                To: Genetics Psittacine <genetics-psittacine@yahoogroups.com>
                                Sent: Saturday, August 4, 2012 2:51 PM
                                Subject: Fw: [Genetics-Psittacine] Parblues IRN do not exist
                                 
                                 
                                Sorry, correction
                                 
                                Sent: Saturday, August 04, 2012 2:34 PM
                                Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                 
                                 
                                We are trying to align natural events within boundaries/divisions we have created, instead of the other way round. This all in an effort to understand things according to present knowledge.
                                What we have seen lately, is the fading of man-made boundaries in established man-made classification systems with the advances in and release of knowledge. As an example, look at the definitions for inheritance behaviour; dominant, recessive etc. We live in a changing world and so we have to adapt and start thinking about the inadequacies of established systems and start formulating new criteria and new directions of thinking, considering what we know today and what we believe we know.
                                 
                                Look at the man-made divisions in the development of a new life in legal definitions of when a developing new individual may be executed through legal abortion, decided on by Someone playing God that is putting up divisions in a process of programmed continuing development.
                                 
                                A homozygotic parblue can never be phenotypically wild-type. Even with 80% psittacin retention in a homoallelic homozygous event, there is still a 20% loss of...exactly what? Quantitative decrease of psittacins as a collective homogenous mass of different psittacins? What about the quality, where are the control points for facets of psittacins; colour tone, brilliance, hue, interactions, all the possible modifications, the millions of available colour expressions. The exchange of one metal molecule for another in the white paper for colour production, brought about by a single base substitution and the major effect of such a minute alteration.
                                 
                                Deon
                                 
                                Sent: Saturday, August 04, 2012 12:52 PM
                                Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                 
                                 
                                Peter, Deon, Terry, Wynand, .... every other with knowledge in "the smart stuff",
                                 
                                I have checked that the definitions of homoalleles and heteroalleles made by Terry are correct... but I have a problem for understanding it : it seems that the changes in nucleotide composition in one specific part of a gene will always produce a change in the quantity of the RNAm produced ... a change in the quantity of the protein produced ... a quantitatif change in the final effect we see .... but changes in a different part of the same gene will finally produce,  by a similar mechanisms, quantitatif changes in a different final effect that we see. In fact it seems that those heteroalleles act as if they were consecutive genes, but, I guess, without a stop codon. Is it the case? If it is the case ... how can we make the difference between two extremely linked genes and two heteroalleles? ... and which would be the functional differences allowing for identification of one or another?
                                 
                                First problem : most of the proteins involved in colour regulation are enzymes. The activity of enzymes is highly dependent on its tridimensional structure, and this structure depends mainly on the disposition of some specific aminoacids (those showing an asymetric -NH3 or -COOH), hydrogen bridges, ... that is, on the repartition of electric charges. A change in just one aminoacid can completely change the tridimensional structure of the enzyme and, thus, its activity. We can have different mutations acting at the same point of the gene. Some of them will be able to induce little changes, if any, in the final expression allowing for a change in the quantitatif final effect (classical homoalleles), but others, acting on the same point could induce a big change in the spatial configuration allowing the production of a different enzyme with or without a functional activity. So the same point of the same gene could produce apparent homoalleles and heteroalleles.
                                 
                                Second problem: In the same way I can imagine that mutations acting in different parts of the same gene, could lead to a similar final tridimensional structure of the enzyme, producing just a little change in the quantitatif production of the final effect, as if both mutations were homoallelic, despite that they are acting on different points of the same gene.
                                 
                                So, how can we say if two alleles behave as homoalleles or as heteroalleles without genetic studies? Which are the criteria to assume one or the other?
                                 
                                Regards
                                 
                                Recio
                                 






                              • Deon Smith
                                Recio said: ...the concept of wild allele should be changed by the concept of prevalent allele in a given population. This is technically correct but what
                                Message 15 of 27 , Aug 5 6:48 AM
                                  Recio said:  ...the concept of wild allele should be changed by the concept of "prevalent" allele in a given population.
                                   
                                  This is technically correct but what reality examples do you have of this? Terry mentioned in his last postings the situation where a mutation actually replaced the wild-type, I think it was an Opaline Stella or something, but this was in a captive environment. The concept of wild-type will remain valid ad infinitum, you must be careful not to confuse people!
                                   
                                  I get the idea you want to promote, but it is a pity you could not use Lutino, a simple single mutation instead of a combo type but your idea is sound and I am glad to say a perfect demonstration of my philosophical remarks about new trends in thinking and an open mind, new perceptions, not taking existing perceptions as holy cows.
                                   
                                  I believe wild-type will remain the reference standard forever, do you foresee anything else replacing it in the next 100000 years?
                                   
                                  Deon
                                   
                                  Sent: Sunday, August 05, 2012 2:29 PM
                                  Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                   
                                   

                                  Hi Deon,
                                   
                                  You have explained some of the possibilities to explain results at the genetic level. You could even add transformations of the initially produced protein so that it is sliced in different proteins with different functions, even that they come all of them from the same gene (Ex: proopiomelanocortin producing several hormones and peptides : http://en.wikipedia.org/wiki/Proopiomelanocortin) ... but the question remains intact :
                                   
                                  If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele?
                                   
                                  I will tell you a history so you will understand that wild alleles do not "exist" (as well as mutated alleles) :
                                  Recio was a selfconfident man leaving in Whiteland. In Whiteland every animal was white because of the white environement due to snow : there were white rabbits, white mice, .... and wild IRNs with a white phenotype and black eyes who had wonderfully adapted to the environement centuries ago. From men memory these birds had always been there, and they were even represented in the oldest totems that archeologist have found. Recio detected that from time to time there were spontanous mutations in the white wild IRN producing strange birds who were called dom pied IRN, since the mutation acted as dominant and the birds showed a patched expression of melanin. Some bird breeders in Whiteland had even proven that whenever two heterozygous birds were paired, they could get a strange mutant showing a green phenotype. Thus the homozygous form of the dom pied mutation was called green mutant.
                                  At the time the first green mutant was detected Recio contacted his friend Deon who was living in a warm country and was also a bird hobby man. He sent to him some pics of the wild bird (white phenotype), the heterozygous bird (dom pied) and the homozygous bird (green mutant) telling to Deon that this strange mutation behaves as incomplete dominant. When Deon received the pics with the labelled mutations, he was sure that Recio had made a mistake when labeling the pics, because in his country the wild bird was green and the homozygous mutation was white.
                                   
                                  Tell me my friends ... who of both Recio or Deon was right? Were both right? This is my feeling .... and if both of them were right it means that the concept of wild allele should be changed by the concept of "prevalent" allele in a given population. If the different alleles of a gene are considered in a "democratic" way, with all of them having the same "importance", we will accpet easierly that what can happen to one of them, can happen to any other. Thus our initial question ....
                                   
                                  If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele?
                                   
                                  .... could be reformuleted as follows:
                                   
                                  If a homozygous homoallelic event appears phenotypically identical to the mutant type, does it represent an allele at all, different to the mutant-type allele?
                                   
                                  We have changed wild by mutant (which in fact is the same as we have seen) and now it seems easier to reformulate the question as : could we get the same phenotypic expression from two different homozygous mutant alleles?
                                   
                                  What's you feeling?
                                   
                                  Recio
                                   
                                  From: Deon Smith <gms1@...>
                                  To: Genetics-Psittacine@yahoogroups.com
                                  Sent: Sunday, August 5, 2012 12:40 AM
                                  Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                   
                                   
                                  To get back to basics: a gene is a functional unit of heredity. It is a segment of DNA that is responsible for the physical and inheritable characteristics or phenotype of a living organism.A gene is made up of sequences of base pairs of variable length, where each base pair may potentially be subject to mutation; each base pair being physically able to have 3 different alleles of forms, apart from the wild type allele. But a gene may span many many base pairs. Your quotation of Terry’s definition and Peter’s interpretation is spot on, but the crucial word is functional. When we get to functional units we have to address exons and introns which I will  not go into now, suffice to say that a functional unit of a gene codes for specific proteins and enzymes, which may be changed by different modifiers and mutations.
                                  Due to the complexity of gene structure, different segments of a gene may mutate, giving origin to different alleles which may appear (act) like another gene, in which case we talk of heteroalleles. When the same functional unit is involved, we get homoallelic relations.
                                   
                                  The control of psittacins in toto must be a massive task for one or two genes, with very little research results available on commercially-directed studies on poultry as an example. We must assume that more than one gene, or many, may be involved, given the complexity of psittacin production that must be in place, and that these genes may be massive in size, with many functional segments but still forming part on a specified gene. Read the first sentence again.
                                   
                                  If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele? How will this then be proven?
                                   
                                  I believe that the expression of the normal wildtype allele is the normal state and not an additional expense of energy, therefore mutations at these loci are inhibitory in nature and the homozygote appears closer to the normal wildtype phenotype, unless we have a situation where the homozygotic form appears closer to the complete mutation than the heterozygote, that we see in other spp. But in this latter instance we must not overlook epistasis in the heterozygote, where one gene could code for a protein preventing transcription of the other gene. Also, epistasis must be differentiated from dominance at the homoallelic level that points to an interaction between alleles at the same gene functional unit. And not the least, intragenic complementation but this must refer to heteroalleles which is not applicable here, it refers to two alleles complementing in the heteroallelic event; we are referring to a homoallelic difference, unless we have an unexpected situation of heteroalleles, other than in the ringneck. These 3 functional options may all explain the phenomenon where the homozygote appears closer to the complete mutation allele than the heterozygote.
                                   
                                  Deon
                                   
                                   
                                   
                                   
                                   
                                   
                                  Sent: Saturday, August 04, 2012 8:54 PM
                                  Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                   
                                   
                                  Hi Deon,
                                   
                                  I adept completely to the phylosophical part (even and specially to the criteria of begining of life) ... but this forum is about a different subject.
                                   
                                  A homozygotic parblue can never be phenotypically wild-type. Are you sure? Remember what you have just written : We live in a changing world and so we have to adapt and start thinking about the inadequacies of established systems and start formulating new criteria and new directions of thinking, considering what we know today and what we believe we know.
                                  I think that it depends whether this parblue acts through an inhibitory mechanism (then you would be rigth) or through an activatory mechanism (then your sentence would not be correct). Imagine a parblue mutation able to decrease the final psittacine of 40% (it means that 60% of the psittacine is expressed) when only one allele of this parblue is expressed (Ex ParblueBlue).
                                   
                                  1. If activatory mechanism :
                                  WildParblue ..... wild phenotype
                                  ParblueBlue ..... parblue phenotype (psittacine expression of 60% since there is only an activation of 60% of the system leading to psittacin production)
                                  ParblueParblue ..... wild phenotype since the theoretical capacity of psittacine production is 120% (60% from each Parblue allele) .... wild phenotype.
                                   
                                  2. If inhibitory mechanism:
                                  WildParblue ..... wild phenotype.
                                  ParblueBlue ..... parblue phenotype (psittacine expression of 60% since there is a block of 40% in the capacity of the metabolic path leading to psittacin production due to the increase in the production of an inhibitory agent).
                                  ParblueParblue ..... parblue phenotype expressing only 20%. The homozygous form of the Parblue only expresses 20% since each Parblue allele blocks 40% of the expression. This is a bluish phenotype.
                                   
                                  So, for a Parblue mutation able to express more than 50% of the final product when it is present in the heterozygous form (BlueParblue) and acting through an activatory mechanism, it would be posible to get an apparent wild phenotype in the homozygous form (ParblueParblue). Please, if you think that I am wrong .... could you tell me specifically why/where in my reasoning?
                                   
                                  Why everybody accepts the same reasoning for an activatory mechanism if the parblue mutation expresses less than 50% of the final product (let's say 30%) in the heterozygous form, so that in the homozygous form (60% of psittacin expression) we get a greener bird with less than 100% expression, that is a heavy parblue? Is this reasoning valid only when it conforts our previous ideas? Let's open our minds ... and if I am wrong ... let me know it .... with reasons.
                                   
                                  Maybe the problem is that you are thinking that the mutated genes are the same for both mechanisms ... but this is wrong : only in the activatory mechanism we can properly speak of parblues because the partially mutated gene is the same which completely blocks psittacin production (Blue). In the inhibitory mechanism the mutated gene is different. It is coding for a different enzyme, acting by an inhibitory mechanism in psittacine synthesis ... and this is the reason that I said that we can not compare two apparent parblues mutations in different species when the homozygous parblues behave differently (greener in one specie and bluer in the other).
                                   
                                  Even with 80% psittacin retention in a homoallelic homozygous event, there is still a 20% loss of...exactly what? Quantitative decrease of psittacins as a collective homogenous mass of different psittacins? What about the quality, where are the control points for facets of psittacins; colour tone, brilliance, hue, interactions, all the possible modifications, the millions of available colour expressions.
                                   
                                  I agree ... and this is why we are here.... trying to approach the "truth", even that our models are too simple. Knowledge is like a sphere : when it increases, the number of external points touching the "unknown" also increase, and this is why the most knowledgable people are those with more doubts and questions. I am sure that some of the persons who doubt the most here are Terry and Inte ... and that this is the reason their presence is rare : we can not answer their questions ... but our questions could trigger new ideas in their minds, so they both should be a little more presents.
                                   
                                  Regards
                                   
                                  Recio
                                  From: Deon Smith <gms1@...>
                                  To: Genetics Psittacine <genetics-psittacine@yahoogroups.com>
                                  Sent: Saturday, August 4, 2012 2:51 PM
                                  Subject: Fw: [Genetics-Psittacine] Parblues IRN do not exist
                                   
                                   
                                  Sorry, correction
                                   
                                  Sent: Saturday, August 04, 2012 2:34 PM
                                  Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                   
                                   
                                  We are trying to align natural events within boundaries/divisions we have created, instead of the other way round. This all in an effort to understand things according to present knowledge.
                                  What we have seen lately, is the fading of man-made boundaries in established man-made classification systems with the advances in and release of knowledge. As an example, look at the definitions for inheritance behaviour; dominant, recessive etc. We live in a changing world and so we have to adapt and start thinking about the inadequacies of established systems and start formulating new criteria and new directions of thinking, considering what we know today and what we believe we know.
                                   
                                  Look at the man-made divisions in the development of a new life in legal definitions of when a developing new individual may be executed through legal abortion, decided on by Someone playing God that is putting up divisions in a process of programmed continuing development.
                                   
                                  A homozygotic parblue can never be phenotypically wild-type. Even with 80% psittacin retention in a homoallelic homozygous event, there is still a 20% loss of...exactly what? Quantitative decrease of psittacins as a collective homogenous mass of different psittacins? What about the quality, where are the control points for facets of psittacins; colour tone, brilliance, hue, interactions, all the possible modifications, the millions of available colour expressions. The exchange of one metal molecule for another in the white paper for colour production, brought about by a single base substitution and the major effect of such a minute alteration.
                                   
                                  Deon
                                   
                                  Sent: Saturday, August 04, 2012 12:52 PM
                                  Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                   
                                   
                                  Peter, Deon, Terry, Wynand, .... every other with knowledge in "the smart stuff",
                                   
                                  I have checked that the definitions of homoalleles and heteroalleles made by Terry are correct... but I have a problem for understanding it : it seems that the changes in nucleotide composition in one specific part of a gene will always produce a change in the quantity of the RNAm produced ... a change in the quantity of the protein produced ... a quantitatif change in the final effect we see .... but changes in a different part of the same gene will finally produce,  by a similar mechanisms, quantitatif changes in a different final effect that we see. In fact it seems that those heteroalleles act as if they were consecutive genes, but, I guess, without a stop codon. Is it the case? If it is the case ... how can we make the difference between two extremely linked genes and two heteroalleles? ... and which would be the functional differences allowing for identification of one or another?
                                   
                                  First problem : most of the proteins involved in colour regulation are enzymes. The activity of enzymes is highly dependent on its tridimensional structure, and this structure depends mainly on the disposition of some specific aminoacids (those showing an asymetric -NH3 or -COOH), hydrogen bridges, ... that is, on the repartition of electric charges. A change in just one aminoacid can completely change the tridimensional structure of the enzyme and, thus, its activity. We can have different mutations acting at the same point of the gene. Some of them will be able to induce little changes, if any, in the final expression allowing for a change in the quantitatif final effect (classical homoalleles), but others, acting on the same point could induce a big change in the spatial configuration allowing the production of a different enzyme with or without a functional activity. So the same point of the same gene could produce apparent homoalleles and heteroalleles.
                                   
                                  Second problem: In the same way I can imagine that mutations acting in different parts of the same gene, could lead to a similar final tridimensional structure of the enzyme, producing just a little change in the quantitatif production of the final effect, as if both mutations were homoallelic, despite that they are acting on different points of the same gene.
                                   
                                  So, how can we say if two alleles behave as homoalleles or as heteroalleles without genetic studies? Which are the criteria to assume one or the other?
                                   
                                  Regards
                                   
                                  Recio
                                   




                                • Peter Wouters
                                  Hi Guys, I would reffer to the Gouldian finch. There are three headcolors in the wild. Redhead, Blackhead and Orange. Long it was thought that the Blackhead
                                  Message 16 of 27 , Aug 5 7:47 AM
                                    Hi Guys,
                                     
                                    I would reffer to the Gouldian finch. There are three headcolors in the wild. Redhead, Blackhead and Orange. Long it was thought that the Blackhead Gould(recessive sexlinked) was the original wildtype because of his majority. Today it is generally accepted that the Redhead(Dominant sexlinked) was the original wildtype. This is an example where a mutation replaces the wildtype, but I’m not sure whether they are on the same locus.
                                     
                                    Regards
                                    Peter 
                                     
                                    Sent: Sunday, August 05, 2012 3:48 PM
                                    Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                     
                                     

                                    Recio said:  ...the concept of wild allele should be changed by the concept of "prevalent" allele in a given population.
                                     
                                    This is technically correct but what reality examples do you have of this? Terry mentioned in his last postings the situation where a mutation actually replaced the wild-type, I think it was an Opaline Stella or something, but this was in a captive environment. The concept of wild-type will remain valid ad infinitum, you must be careful not to confuse people!
                                     
                                    I get the idea you want to promote, but it is a pity you could not use Lutino, a simple single mutation instead of a combo type but your idea is sound and I am glad to say a perfect demonstration of my philosophical remarks about new trends in thinking and an open mind, new perceptions, not taking existing perceptions as holy cows.
                                     
                                    I believe wild-type will remain the reference standard forever, do you foresee anything else replacing it in the next 100000 years?
                                     
                                    Deon
                                     
                                    Sent: Sunday, August 05, 2012 2:29 PM
                                    Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                     
                                     

                                    Hi Deon,
                                     
                                    You have explained some of the possibilities to explain results at the genetic level. You could even add transformations of the initially produced protein so that it is sliced in different proteins with different functions, even that they come all of them from the same gene (Ex: proopiomelanocortin producing several hormones and peptides : http://en.wikipedia.org/wiki/Proopiomelanocortin) ... but the question remains intact :
                                     
                                    If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele?
                                     
                                    I will tell you a history so you will understand that wild alleles do not "exist" (as well as mutated alleles) :
                                    Recio was a selfconfident man leaving in Whiteland. In Whiteland every animal was white because of the white environement due to snow : there were white rabbits, white mice, .... and wild IRNs with a white phenotype and black eyes who had wonderfully adapted to the environement centuries ago. From men memory these birds had always been there, and they were even represented in the oldest totems that archeologist have found. Recio detected that from time to time there were spontanous mutations in the white wild IRN producing strange birds who were called dom pied IRN, since the mutation acted as dominant and the birds showed a patched expression of melanin. Some bird breeders in Whiteland had even proven that whenever two heterozygous birds were paired, they could get a strange mutant showing a green phenotype. Thus the homozygous form of the dom pied mutation was called green mutant.
                                    At the time the first green mutant was detected Recio contacted his friend Deon who was living in a warm country and was also a bird hobby man. He sent to him some pics of the wild bird (white phenotype), the heterozygous bird (dom pied) and the homozygous bird (green mutant) telling to Deon that this strange mutation behaves as incomplete dominant. When Deon received the pics with the labelled mutations, he was sure that Recio had made a mistake when labeling the pics, because in his country the wild bird was green and the homozygous mutation was white.
                                     
                                    Tell me my friends ... who of both Recio or Deon was right? Were both right? This is my feeling .... and if both of them were right it means that the concept of wild allele should be changed by the concept of "prevalent" allele in a given population. If the different alleles of a gene are considered in a "democratic" way, with all of them having the same "importance", we will accpet easierly that what can happen to one of them, can happen to any other. Thus our initial question ....
                                     
                                    If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele?
                                     
                                    .... could be reformuleted as follows:
                                     
                                    If a homozygous homoallelic event appears phenotypically identical to the mutant type, does it represent an allele at all, different to the mutant-type allele?
                                     
                                    We have changed wild by mutant (which in fact is the same as we have seen) and now it seems easier to reformulate the question as : could we get the same phenotypic expression from two different homozygous mutant alleles?
                                     
                                    What's you feeling?
                                     
                                    Recio
                                     
                                    From: Deon Smith <gms1@...>
                                    To: Genetics-Psittacine@yahoogroups.com
                                    Sent: Sunday, August 5, 2012 12:40 AM
                                    Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                     
                                     
                                    To get back to basics: a gene is a functional unit of heredity. It is a segment of DNA that is responsible for the physical and inheritable characteristics or phenotype of a living organism.A gene is made up of sequences of base pairs of variable length, where each base pair may potentially be subject to mutation; each base pair being physically able to have 3 different alleles of forms, apart from the wild type allele. But a gene may span many many base pairs. Your quotation of Terry’s definition and Peter’s interpretation is spot on, but the crucial word is functional. When we get to functional units we have to address exons and introns which I will  not go into now, suffice to say that a functional unit of a gene codes for specific proteins and enzymes, which may be changed by different modifiers and mutations.
                                    Due to the complexity of gene structure, different segments of a gene may mutate, giving origin to different alleles which may appear (act) like another gene, in which case we talk of heteroalleles. When the same functional unit is involved, we get homoallelic relations.
                                     
                                    The control of psittacins in toto must be a massive task for one or two genes, with very little research results available on commercially-directed studies on poultry as an example. We must assume that more than one gene, or many, may be involved, given the complexity of psittacin production that must be in place, and that these genes may be massive in size, with many functional segments but still forming part on a specified gene. Read the first sentence again.
                                     
                                    If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele? How will this then be proven?
                                     
                                    I believe that the expression of the normal wildtype allele is the normal state and not an additional expense of energy, therefore mutations at these loci are inhibitory in nature and the homozygote appears closer to the normal wildtype phenotype, unless we have a situation where the homozygotic form appears closer to the complete mutation than the heterozygote, that we see in other spp. But in this latter instance we must not overlook epistasis in the heterozygote, where one gene could code for a protein preventing transcription of the other gene. Also, epistasis must be differentiated from dominance at the homoallelic level that points to an interaction between alleles at the same gene functional unit. And not the least, intragenic complementation but this must refer to heteroalleles which is not applicable here, it refers to two alleles complementing in the heteroallelic event; we are referring to a homoallelic difference, unless we have an unexpected situation of heteroalleles, other than in the ringneck. These 3 functional options may all explain the phenomenon where the homozygote appears closer to the complete mutation allele than the heterozygote.
                                     
                                    Deon
                                     
                                     
                                     
                                     
                                     
                                     
                                    Sent: Saturday, August 04, 2012 8:54 PM
                                    Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                     
                                     
                                    Hi Deon,
                                     
                                    I adept completely to the phylosophical part (even and specially to the criteria of begining of life) ... but this forum is about a different subject.
                                     
                                    A homozygotic parblue can never be phenotypically wild-type. Are you sure? Remember what you have just written : We live in a changing world and so we have to adapt and start thinking about the inadequacies of established systems and start formulating new criteria and new directions of thinking, considering what we know today and what we believe we know.
                                    I think that it depends whether this parblue acts through an inhibitory mechanism (then you would be rigth) or through an activatory mechanism (then your sentence would not be correct). Imagine a parblue mutation able to decrease the final psittacine of 40% (it means that 60% of the psittacine is expressed) when only one allele of this parblue is expressed (Ex ParblueBlue).
                                     
                                    1. If activatory mechanism :
                                    WildParblue ..... wild phenotype
                                    ParblueBlue ..... parblue phenotype (psittacine expression of 60% since there is only an activation of 60% of the system leading to psittacin production)
                                    ParblueParblue ..... wild phenotype since the theoretical capacity of psittacine production is 120% (60% from each Parblue allele) .... wild phenotype.
                                     
                                    2. If inhibitory mechanism:
                                    WildParblue ..... wild phenotype.
                                    ParblueBlue ..... parblue phenotype (psittacine expression of 60% since there is a block of 40% in the capacity of the metabolic path leading to psittacin production due to the increase in the production of an inhibitory agent).
                                    ParblueParblue ..... parblue phenotype expressing only 20%. The homozygous form of the Parblue only expresses 20% since each Parblue allele blocks 40% of the expression. This is a bluish phenotype.
                                     
                                    So, for a Parblue mutation able to express more than 50% of the final product when it is present in the heterozygous form (BlueParblue) and acting through an activatory mechanism, it would be posible to get an apparent wild phenotype in the homozygous form (ParblueParblue). Please, if you think that I am wrong .... could you tell me specifically why/where in my reasoning?
                                     
                                    Why everybody accepts the same reasoning for an activatory mechanism if the parblue mutation expresses less than 50% of the final product (let's say 30%) in the heterozygous form, so that in the homozygous form (60% of psittacin expression) we get a greener bird with less than 100% expression, that is a heavy parblue? Is this reasoning valid only when it conforts our previous ideas? Let's open our minds ... and if I am wrong ... let me know it .... with reasons.
                                     
                                    Maybe the problem is that you are thinking that the mutated genes are the same for both mechanisms ... but this is wrong : only in the activatory mechanism we can properly speak of parblues because the partially mutated gene is the same which completely blocks psittacin production (Blue). In the inhibitory mechanism the mutated gene is different. It is coding for a different enzyme, acting by an inhibitory mechanism in psittacine synthesis ... and this is the reason that I said that we can not compare two apparent parblues mutations in different species when the homozygous parblues behave differently (greener in one specie and bluer in the other).
                                     
                                    Even with 80% psittacin retention in a homoallelic homozygous event, there is still a 20% loss of...exactly what? Quantitative decrease of psittacins as a collective homogenous mass of different psittacins? What about the quality, where are the control points for facets of psittacins; colour tone, brilliance, hue, interactions, all the possible modifications, the millions of available colour expressions.
                                     
                                    I agree ... and this is why we are here.... trying to approach the "truth", even that our models are too simple. Knowledge is like a sphere : when it increases, the number of external points touching the "unknown" also increase, and this is why the most knowledgable people are those with more doubts and questions. I am sure that some of the persons who doubt the most here are Terry and Inte ... and that this is the reason their presence is rare : we can not answer their questions ... but our questions could trigger new ideas in their minds, so they both should be a little more presents.
                                     
                                    Regards
                                     
                                    Recio
                                    From: Deon Smith <gms1@...>
                                    To: Genetics Psittacine <genetics-psittacine@yahoogroups.com>
                                    Sent: Saturday, August 4, 2012 2:51 PM
                                    Subject: Fw: [Genetics-Psittacine] Parblues IRN do not exist
                                     
                                     
                                    Sorry, correction
                                     
                                    Sent: Saturday, August 04, 2012 2:34 PM
                                    Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                     
                                     
                                    We are trying to align natural events within boundaries/divisions we have created, instead of the other way round. This all in an effort to understand things according to present knowledge.
                                    What we have seen lately, is the fading of man-made boundaries in established man-made classification systems with the advances in and release of knowledge. As an example, look at the definitions for inheritance behaviour; dominant, recessive etc. We live in a changing world and so we have to adapt and start thinking about the inadequacies of established systems and start formulating new criteria and new directions of thinking, considering what we know today and what we believe we know.
                                     
                                    Look at the man-made divisions in the development of a new life in legal definitions of when a developing new individual may be executed through legal abortion, decided on by Someone playing God that is putting up divisions in a process of programmed continuing development.
                                     
                                    A homozygotic parblue can never be phenotypically wild-type. Even with 80% psittacin retention in a homoallelic homozygous event, there is still a 20% loss of...exactly what? Quantitative decrease of psittacins as a collective homogenous mass of different psittacins? What about the quality, where are the control points for facets of psittacins; colour tone, brilliance, hue, interactions, all the possible modifications, the millions of available colour expressions. The exchange of one metal molecule for another in the white paper for colour production, brought about by a single base substitution and the major effect of such a minute alteration.
                                     
                                    Deon
                                     
                                    Sent: Saturday, August 04, 2012 12:52 PM
                                    Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                     
                                     
                                    Peter, Deon, Terry, Wynand, .... every other with knowledge in "the smart stuff",
                                     
                                    I have checked that the definitions of homoalleles and heteroalleles made by Terry are correct... but I have a problem for understanding it : it seems that the changes in nucleotide composition in one specific part of a gene will always produce a change in the quantity of the RNAm produced ... a change in the quantity of the protein produced ... a quantitatif change in the final effect we see .... but changes in a different part of the same gene will finally produce,  by a similar mechanisms, quantitatif changes in a different final effect that we see. In fact it seems that those heteroalleles act as if they were consecutive genes, but, I guess, without a stop codon. Is it the case? If it is the case ... how can we make the difference between two extremely linked genes and two heteroalleles? ... and which would be the functional differences allowing for identification of one or another?
                                     
                                    First problem : most of the proteins involved in colour regulation are enzymes. The activity of enzymes is highly dependent on its tridimensional structure, and this structure depends mainly on the disposition of some specific aminoacids (those showing an asymetric -NH3 or -COOH), hydrogen bridges, ... that is, on the repartition of electric charges. A change in just one aminoacid can completely change the tridimensional structure of the enzyme and, thus, its activity. We can have different mutations acting at the same point of the gene. Some of them will be able to induce little changes, if any, in the final expression allowing for a change in the quantitatif final effect (classical homoalleles), but others, acting on the same point could induce a big change in the spatial configuration allowing the production of a different enzyme with or without a functional activity. So the same point of the same gene could produce apparent homoalleles and heteroalleles.
                                     
                                    Second problem: In the same way I can imagine that mutations acting in different parts of the same gene, could lead to a similar final tridimensional structure of the enzyme, producing just a little change in the quantitatif production of the final effect, as if both mutations were homoallelic, despite that they are acting on different points of the same gene.
                                     
                                    So, how can we say if two alleles behave as homoalleles or as heteroalleles without genetic studies? Which are the criteria to assume one or the other?
                                     
                                    Regards
                                     
                                    Recio
                                     




                                  • Recio Joaquin
                                    Hi Deon,   The truth of the last tale is that Recio was in Yellowland and Deon in Blueland ...   The concept of wild-type will remain valid ad infinitum ...
                                    Message 17 of 27 , Aug 5 8:05 AM
                                      Hi Deon,
                                       
                                      The truth of the last tale is that Recio was in Yellowland and Deon in Blueland ...
                                       
                                      The concept of wild-type will remain valid ad infinitum ... yes for the concept but not for the wild type which will evolve with environemental changing conditions, even if they are very slow for a man life span.
                                       
                                      The concept of wild type is valid to know what we are speaking about, since it gives us a reference bird to describe mutations. But it does not mean that the wild allele is different of the other alleles, and depending on the considered genes, the wild allele will act as recesive (genes coding for feather structure showing dominant mutants) or as dominant (genes coding for pigments production showing recessive mutations).
                                       
                                      We should begin to think about alleles as different functional possibilities of a gen, and we should begin to think about dominance or recessivity as the relations of expressivity of the different functional possibilities of a gen: the same allele could behave as dominant or as recessive depending on which is the other allele considered in the pair.
                                      Ex: Let's imagine a bird species with 3 different alleles producing 0, 20 and 40 units of a pigment each (alleles P-0, P-20 and P-40).
                                       
                                      If we consider a population owing only P-0 and P-20 we could find the following possibilities:
                                      1. P-0P-0 .... bird without pigment
                                      2. P-20P-20 .... bird producing 40 units of pigment
                                      2. P-0P-20 .... 3 possibilities:
                                              P-0 behaves as dominant or P-20 behaves as recessive ..... no pigment
                                              P-0 and P-20 behave as incomplete dominants .... 10 units of pigment
                                              P0 behaves as recessive and P-20 behaves as dominant .... 20 units of pigment
                                       
                                      If this system is saturated at 20 units (many possible reasons from translation to final expression) P-20P-20 phenotype will be the same than P-0P-20 whenever P-20 behaves as dominant. We will say that P-20 behaves as dominant.
                                       
                                      If the system is not saturated at 20 units but at 40 or more units of pigment, we will say that P-20 behaves as incomplete dominant.
                                       
                                      If the system is saturated at 10 units the phenotypic expression of P-20P-20 and P-0P-20 will be the same for P-20 acting both as dominant or as incomplete dominant. We will say that -20 is dominant.
                                       
                                      You can do a similar reasoning for a population owing only P-20 and P-40, and you will notice that P-20 (which could act as dominant or incomplete dominant in the first population) can act as recessive in the second population.
                                       
                                      As you can see an allele is not dominant or incomplete dominant or recessive, but it depends on to which other allele he is paired and the conditions of saturability of its expression.
                                       
                                      Of course these are theoretical considerations and if you ask me for examples in real life I will say "I do not know, I am not an expert", but these theoretical considerations show that we could get, at least in theory, a wild phenotype as the expression of an homozygous homoallelic mutant.... and conforts the hypothesis of a heavy turquoise as the wild phenotypic expression of the gene coding for patched psittacin.
                                       
                                      Regards
                                       
                                      Recio
                                       
                                      From: Deon Smith <gms1@...>
                                      To: Genetics-Psittacine@yahoogroups.com
                                      Sent: Sunday, August 5, 2012 3:48 PM
                                      Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist

                                       
                                      Recio said:  ...the concept of wild allele should be changed by the concept of "prevalent" allele in a given population.
                                       
                                      This is technically correct but what reality examples do you have of this? Terry mentioned in his last postings the situation where a mutation actually replaced the wild-type, I think it was an Opaline Stella or something, but this was in a captive environment. The concept of wild-type will remain valid ad infinitum, you must be careful not to confuse people!
                                       
                                      I get the idea you want to promote, but it is a pity you could not use Lutino, a simple single mutation instead of a combo type but your idea is sound and I am glad to say a perfect demonstration of my philosophical remarks about new trends in thinking and an open mind, new perceptions, not taking existing perceptions as holy cows.
                                       
                                      I believe wild-type will remain the reference standard forever, do you foresee anything else replacing it in the next 100000 years?
                                       
                                      Deon
                                       
                                      Sent: Sunday, August 05, 2012 2:29 PM
                                      Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                       
                                       
                                      Hi Deon,
                                       
                                      You have explained some of the possibilities to explain results at the genetic level. You could even add transformations of the initially produced protein so that it is sliced in different proteins with different functions, even that they come all of them from the same gene (Ex: proopiomelanocortin producing several hormones and peptides : http://en.wikipedia.org/wiki/Proopiomelanocortin) ... but the question remains intact :
                                       
                                      If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele?
                                       
                                      I will tell you a history so you will understand that wild alleles do not "exist" (as well as mutated alleles) :
                                      Recio was a selfconfident man leaving in Whiteland. In Whiteland every animal was white because of the white environement due to snow : there were white rabbits, white mice, .... and wild IRNs with a white phenotype and black eyes who had wonderfully adapted to the environement centuries ago. From men memory these birds had always been there, and they were even represented in the oldest totems that archeologist have found. Recio detected that from time to time there were spontanous mutations in the white wild IRN producing strange birds who were called dom pied IRN, since the mutation acted as dominant and the birds showed a patched expression of melanin. Some bird breeders in Whiteland had even proven that whenever two heterozygous birds were paired, they could get a strange mutant showing a green phenotype. Thus the homozygous form of the dom pied mutation was called green mutant.
                                      At the time the first green mutant was detected Recio contacted his friend Deon who was living in a warm country and was also a bird hobby man. He sent to him some pics of the wild bird (white phenotype), the heterozygous bird (dom pied) and the homozygous bird (green mutant) telling to Deon that this strange mutation behaves as incomplete dominant. When Deon received the pics with the labelled mutations, he was sure that Recio had made a mistake when labeling the pics, because in his country the wild bird was green and the homozygous mutation was white.
                                       
                                      Tell me my friends ... who of both Recio or Deon was right? Were both right? This is my feeling .... and if both of them were right it means that the concept of wild allele should be changed by the concept of "prevalent" allele in a given population. If the different alleles of a gene are considered in a "democratic" way, with all of them having the same "importance", we will accpet easierly that what can happen to one of them, can happen to any other. Thus our initial question ....
                                       
                                      If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele?
                                       
                                      .... could be reformuleted as follows:
                                       
                                      If a homozygous homoallelic event appears phenotypically identical to the mutant type, does it represent an allele at all, different to the mutant-type allele?
                                       
                                      We have changed wild by mutant (which in fact is the same as we have seen) and now it seems easier to reformulate the question as : could we get the same phenotypic expression from two different homozygous mutant alleles?
                                       
                                      What's you feeling?
                                       
                                      Recio
                                       
                                      From: Deon Smith <gms1@...>
                                      To: Genetics-Psittacine@yahoogroups.com
                                      Sent: Sunday, August 5, 2012 12:40 AM
                                      Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                       
                                       
                                      To get back to basics: a gene is a functional unit of heredity. It is a segment of DNA that is responsible for the physical and inheritable characteristics or phenotype of a living organism.A gene is made up of sequences of base pairs of variable length, where each base pair may potentially be subject to mutation; each base pair being physically able to have 3 different alleles of forms, apart from the wild type allele. But a gene may span many many base pairs. Your quotation of Terry’s definition and Peter’s interpretation is spot on, but the crucial word is functional. When we get to functional units we have to address exons and introns which I will  not go into now, suffice to say that a functional unit of a gene codes for specific proteins and enzymes, which may be changed by different modifiers and mutations.
                                      Due to the complexity of gene structure, different segments of a gene may mutate, giving origin to different alleles which may appear (act) like another gene, in which case we talk of heteroalleles. When the same functional unit is involved, we get homoallelic relations.
                                       
                                      The control of psittacins in toto must be a massive task for one or two genes, with very little research results available on commercially-directed studies on poultry as an example. We must assume that more than one gene, or many, may be involved, given the complexity of psittacin production that must be in place, and that these genes may be massive in size, with many functional segments but still forming part on a specified gene. Read the first sentence again.
                                       
                                      If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele? How will this then be proven?
                                       
                                      I believe that the expression of the normal wildtype allele is the normal state and not an additional expense of energy, therefore mutations at these loci are inhibitory in nature and the homozygote appears closer to the normal wildtype phenotype, unless we have a situation where the homozygotic form appears closer to the complete mutation than the heterozygote, that we see in other spp. But in this latter instance we must not overlook epistasis in the heterozygote, where one gene could code for a protein preventing transcription of the other gene. Also, epistasis must be differentiated from dominance at the homoallelic level that points to an interaction between alleles at the same gene functional unit. And not the least, intragenic complementation but this must refer to heteroalleles which is not applicable here, it refers to two alleles complementing in the heteroallelic event; we are referring to a homoallelic difference, unless we have an unexpected situation of heteroalleles, other than in the ringneck. These 3 functional options may all explain the phenomenon where the homozygote appears closer to the complete mutation allele than the heterozygote.
                                       
                                      Deon
                                       
                                       
                                       
                                       
                                       
                                       
                                      Sent: Saturday, August 04, 2012 8:54 PM
                                      Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                       
                                       
                                      Hi Deon,
                                       
                                      I adept completely to the phylosophical part (even and specially to the criteria of begining of life) ... but this forum is about a different subject.
                                       
                                      A homozygotic parblue can never be phenotypically wild-type. Are you sure? Remember what you have just written : We live in a changing world and so we have to adapt and start thinking about the inadequacies of established systems and start formulating new criteria and new directions of thinking, considering what we know today and what we believe we know.
                                      I think that it depends whether this parblue acts through an inhibitory mechanism (then you would be rigth) or through an activatory mechanism (then your sentence would not be correct). Imagine a parblue mutation able to decrease the final psittacine of 40% (it means that 60% of the psittacine is expressed) when only one allele of this parblue is expressed (Ex ParblueBlue).
                                       
                                      1. If activatory mechanism :
                                      WildParblue ..... wild phenotype
                                      ParblueBlue ..... parblue phenotype (psittacine expression of 60% since there is only an activation of 60% of the system leading to psittacin production)
                                      ParblueParblue ..... wild phenotype since the theoretical capacity of psittacine production is 120% (60% from each Parblue allele) .... wild phenotype.
                                       
                                      2. If inhibitory mechanism:
                                      WildParblue ..... wild phenotype.
                                      ParblueBlue ..... parblue phenotype (psittacine expression of 60% since there is a block of 40% in the capacity of the metabolic path leading to psittacin production due to the increase in the production of an inhibitory agent).
                                      ParblueParblue ..... parblue phenotype expressing only 20%. The homozygous form of the Parblue only expresses 20% since each Parblue allele blocks 40% of the expression. This is a bluish phenotype.
                                       
                                      So, for a Parblue mutation able to express more than 50% of the final product when it is present in the heterozygous form (BlueParblue) and acting through an activatory mechanism, it would be posible to get an apparent wild phenotype in the homozygous form (ParblueParblue). Please, if you think that I am wrong .... could you tell me specifically why/where in my reasoning?
                                       
                                      Why everybody accepts the same reasoning for an activatory mechanism if the parblue mutation expresses less than 50% of the final product (let's say 30%) in the heterozygous form, so that in the homozygous form (60% of psittacin expression) we get a greener bird with less than 100% expression, that is a heavy parblue? Is this reasoning valid only when it conforts our previous ideas? Let's open our minds ... and if I am wrong ... let me know it .... with reasons.
                                       
                                      Maybe the problem is that you are thinking that the mutated genes are the same for both mechanisms ... but this is wrong : only in the activatory mechanism we can properly speak of parblues because the partially mutated gene is the same which completely blocks psittacin production (Blue). In the inhibitory mechanism the mutated gene is different. It is coding for a different enzyme, acting by an inhibitory mechanism in psittacine synthesis ... and this is the reason that I said that we can not compare two apparent parblues mutations in different species when the homozygous parblues behave differently (greener in one specie and bluer in the other).
                                       
                                      Even with 80% psittacin retention in a homoallelic homozygous event, there is still a 20% loss of...exactly what? Quantitative decrease of psittacins as a collective homogenous mass of different psittacins? What about the quality, where are the control points for facets of psittacins; colour tone, brilliance, hue, interactions, all the possible modifications, the millions of available colour expressions.
                                       
                                      I agree ... and this is why we are here.... trying to approach the "truth", even that our models are too simple. Knowledge is like a sphere : when it increases, the number of external points touching the "unknown" also increase, and this is why the most knowledgable people are those with more doubts and questions. I am sure that some of the persons who doubt the most here are Terry and Inte ... and that this is the reason their presence is rare : we can not answer their questions ... but our questions could trigger new ideas in their minds, so they both should be a little more presents.
                                       
                                      Regards
                                       
                                      Recio
                                      From: Deon Smith <gms1@...>
                                      To: Genetics Psittacine <genetics-psittacine@yahoogroups.com>
                                      Sent: Saturday, August 4, 2012 2:51 PM
                                      Subject: Fw: [Genetics-Psittacine] Parblues IRN do not exist
                                       
                                       
                                      Sorry, correction
                                       
                                      Sent: Saturday, August 04, 2012 2:34 PM
                                      Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                       
                                       
                                      We are trying to align natural events within boundaries/divisions we have created, instead of the other way round. This all in an effort to understand things according to present knowledge.
                                      What we have seen lately, is the fading of man-made boundaries in established man-made classification systems with the advances in and release of knowledge. As an example, look at the definitions for inheritance behaviour; dominant, recessive etc. We live in a changing world and so we have to adapt and start thinking about the inadequacies of established systems and start formulating new criteria and new directions of thinking, considering what we know today and what we believe we know.
                                       
                                      Look at the man-made divisions in the development of a new life in legal definitions of when a developing new individual may be executed through legal abortion, decided on by Someone playing God that is putting up divisions in a process of programmed continuing development.
                                       
                                      A homozygotic parblue can never be phenotypically wild-type. Even with 80% psittacin retention in a homoallelic homozygous event, there is still a 20% loss of...exactly what? Quantitative decrease of psittacins as a collective homogenous mass of different psittacins? What about the quality, where are the control points for facets of psittacins; colour tone, brilliance, hue, interactions, all the possible modifications, the millions of available colour expressions. The exchange of one metal molecule for another in the white paper for colour production, brought about by a single base substitution and the major effect of such a minute alteration.
                                       
                                      Deon
                                       
                                      Sent: Saturday, August 04, 2012 12:52 PM
                                      Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                       
                                       
                                      Peter, Deon, Terry, Wynand, .... every other with knowledge in "the smart stuff",
                                       
                                      I have checked that the definitions of homoalleles and heteroalleles made by Terry are correct... but I have a problem for understanding it : it seems that the changes in nucleotide composition in one specific part of a gene will always produce a change in the quantity of the RNAm produced ... a change in the quantity of the protein produced ... a quantitatif change in the final effect we see .... but changes in a different part of the same gene will finally produce,  by a similar mechanisms, quantitatif changes in a different final effect that we see. In fact it seems that those heteroalleles act as if they were consecutive genes, but, I guess, without a stop codon. Is it the case? If it is the case ... how can we make the difference between two extremely linked genes and two heteroalleles? ... and which would be the functional differences allowing for identification of one or another?
                                       
                                      First problem : most of the proteins involved in colour regulation are enzymes. The activity of enzymes is highly dependent on its tridimensional structure, and this structure depends mainly on the disposition of some specific aminoacids (those showing an asymetric -NH3 or -COOH), hydrogen bridges, ... that is, on the repartition of electric charges. A change in just one aminoacid can completely change the tridimensional structure of the enzyme and, thus, its activity. We can have different mutations acting at the same point of the gene. Some of them will be able to induce little changes, if any, in the final expression allowing for a change in the quantitatif final effect (classical homoalleles), but others, acting on the same point could induce a big change in the spatial configuration allowing the production of a different enzyme with or without a functional activity. So the same point of the same gene could produce apparent homoalleles and heteroalleles.
                                       
                                      Second problem: In the same way I can imagine that mutations acting in different parts of the same gene, could lead to a similar final tridimensional structure of the enzyme, producing just a little change in the quantitatif production of the final effect, as if both mutations were homoallelic, despite that they are acting on different points of the same gene.
                                       
                                      So, how can we say if two alleles behave as homoalleles or as heteroalleles without genetic studies? Which are the criteria to assume one or the other?
                                       
                                      Regards
                                       
                                      Recio
                                       






                                    • Recio Joaquin
                                      Hi everybody,   I said : You can do a similar reasoning for a population owing only P-20 and P-40, and you will notice that P-20 (which could act as dominant
                                      Message 18 of 27 , Aug 5 8:36 AM
                                        Hi everybody,
                                         
                                        I said : You can do a similar reasoning for a population owing only P-20 and P-40, and you will notice that P-20 (which could act as dominant or incomplete dominant in the first population) can act as recessive in the second population.
                                         
                                        This not true since we can not change the character of dominancy or recessivity depending on the situation we are considering. We can not compare a situation where we consider the allele acting as dominant to a situation where we consider the same allele as recessive.
                                         
                                        Recio

                                        From: Recio Joaquin <jrecio99@...>
                                        To: "Genetics-Psittacine@yahoogroups.com" <Genetics-Psittacine@yahoogroups.com>
                                        Sent: Sunday, August 5, 2012 5:05 PM
                                        Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist

                                         
                                        Hi Deon,
                                         
                                        The truth of the last tale is that Recio was in Yellowland and Deon in Blueland ...
                                         
                                        The concept of wild-type will remain valid ad infinitum ... yes for the concept but not for the wild type which will evolve with environemental changing conditions, even if they are very slow for a man life span.
                                         
                                        The concept of wild type is valid to know what we are speaking about, since it gives us a reference bird to describe mutations. But it does not mean that the wild allele is different of the other alleles, and depending on the considered genes, the wild allele will act as recesive (genes coding for feather structure showing dominant mutants) or as dominant (genes coding for pigments production showing recessive mutations).
                                         
                                        We should begin to think about alleles as different functional possibilities of a gen, and we should begin to think about dominance or recessivity as the relations of expressivity of the different functional possibilities of a gen: the same allele could behave as dominant or as recessive depending on which is the other allele considered in the pair.
                                        Ex: Let's imagine a bird species with 3 different alleles producing 0, 20 and 40 units of a pigment each (alleles P-0, P-20 and P-40).
                                         
                                        If we consider a population owing only P-0 and P-20 we could find the following possibilities:
                                        1. P-0P-0 .... bird without pigment
                                        2. P-20P-20 .... bird producing 40 units of pigment
                                        2. P-0P-20 .... 3 possibilities:
                                                P-0 behaves as dominant or P-20 behaves as recessive ..... no pigment
                                                P-0 and P-20 behave as incomplete dominants .... 10 units of pigment
                                                P0 behaves as recessive and P-20 behaves as dominant .... 20 units of pigment
                                         
                                        If this system is saturated at 20 units (many possible reasons from translation to final expression) P-20P-20 phenotype will be the same than P-0P-20 whenever P-20 behaves as dominant. We will say that P-20 behaves as dominant.
                                         
                                        If the system is not saturated at 20 units but at 40 or more units of pigment, we will say that P-20 behaves as incomplete dominant.
                                         
                                        If the system is saturated at 10 units the phenotypic expression of P-20P-20 and P-0P-20 will be the same for P-20 acting both as dominant or as incomplete dominant. We will say that -20 is dominant.
                                         
                                        You can do a similar reasoning for a population owing only P-20 and P-40, and you will notice that P-20 (which could act as dominant or incomplete dominant in the first population) can act as recessive in the second population.
                                         
                                        As you can see an allele is not dominant or incomplete dominant or recessive, but it depends on to which other allele he is paired and the conditions of saturability of its expression.
                                         
                                        Of course these are theoretical considerations and if you ask me for examples in real life I will say "I do not know, I am not an expert", but these theoretical considerations show that we could get, at least in theory, a wild phenotype as the expression of an homozygous homoallelic mutant.... and conforts the hypothesis of a heavy turquoise as the wild phenotypic expression of the gene coding for patched psittacin.
                                         
                                        Regards
                                         
                                        Recio
                                         
                                        From: Deon Smith <gms1@...>
                                        To: Genetics-Psittacine@yahoogroups.com
                                        Sent: Sunday, August 5, 2012 3:48 PM
                                        Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist

                                         
                                        Recio said:  ...the concept of wild allele should be changed by the concept of "prevalent" allele in a given population.
                                         
                                        This is technically correct but what reality examples do you have of this? Terry mentioned in his last postings the situation where a mutation actually replaced the wild-type, I think it was an Opaline Stella or something, but this was in a captive environment. The concept of wild-type will remain valid ad infinitum, you must be careful not to confuse people!
                                         
                                        I get the idea you want to promote, but it is a pity you could not use Lutino, a simple single mutation instead of a combo type but your idea is sound and I am glad to say a perfect demonstration of my philosophical remarks about new trends in thinking and an open mind, new perceptions, not taking existing perceptions as holy cows.
                                         
                                        I believe wild-type will remain the reference standard forever, do you foresee anything else replacing it in the next 100000 years?
                                         
                                        Deon
                                         
                                        Sent: Sunday, August 05, 2012 2:29 PM
                                        Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                         
                                         
                                        Hi Deon,
                                         
                                        You have explained some of the possibilities to explain results at the genetic level. You could even add transformations of the initially produced protein so that it is sliced in different proteins with different functions, even that they come all of them from the same gene (Ex: proopiomelanocortin producing several hormones and peptides : http://en.wikipedia.org/wiki/Proopiomelanocortin) ... but the question remains intact :
                                         
                                        If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele?
                                         
                                        I will tell you a history so you will understand that wild alleles do not "exist" (as well as mutated alleles) :
                                        Recio was a selfconfident man leaving in Whiteland. In Whiteland every animal was white because of the white environement due to snow : there were white rabbits, white mice, .... and wild IRNs with a white phenotype and black eyes who had wonderfully adapted to the environement centuries ago. From men memory these birds had always been there, and they were even represented in the oldest totems that archeologist have found. Recio detected that from time to time there were spontanous mutations in the white wild IRN producing strange birds who were called dom pied IRN, since the mutation acted as dominant and the birds showed a patched expression of melanin. Some bird breeders in Whiteland had even proven that whenever two heterozygous birds were paired, they could get a strange mutant showing a green phenotype. Thus the homozygous form of the dom pied mutation was called green mutant.
                                        At the time the first green mutant was detected Recio contacted his friend Deon who was living in a warm country and was also a bird hobby man. He sent to him some pics of the wild bird (white phenotype), the heterozygous bird (dom pied) and the homozygous bird (green mutant) telling to Deon that this strange mutation behaves as incomplete dominant. When Deon received the pics with the labelled mutations, he was sure that Recio had made a mistake when labeling the pics, because in his country the wild bird was green and the homozygous mutation was white.
                                         
                                        Tell me my friends ... who of both Recio or Deon was right? Were both right? This is my feeling .... and if both of them were right it means that the concept of wild allele should be changed by the concept of "prevalent" allele in a given population. If the different alleles of a gene are considered in a "democratic" way, with all of them having the same "importance", we will accpet easierly that what can happen to one of them, can happen to any other. Thus our initial question ....
                                         
                                        If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele?
                                         
                                        .... could be reformuleted as follows:
                                         
                                        If a homozygous homoallelic event appears phenotypically identical to the mutant type, does it represent an allele at all, different to the mutant-type allele?
                                         
                                        We have changed wild by mutant (which in fact is the same as we have seen) and now it seems easier to reformulate the question as : could we get the same phenotypic expression from two different homozygous mutant alleles?
                                         
                                        What's you feeling?
                                         
                                        Recio
                                         
                                        From: Deon Smith <gms1@...>
                                        To: Genetics-Psittacine@yahoogroups.com
                                        Sent: Sunday, August 5, 2012 12:40 AM
                                        Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                         
                                         
                                        To get back to basics: a gene is a functional unit of heredity. It is a segment of DNA that is responsible for the physical and inheritable characteristics or phenotype of a living organism.A gene is made up of sequences of base pairs of variable length, where each base pair may potentially be subject to mutation; each base pair being physically able to have 3 different alleles of forms, apart from the wild type allele. But a gene may span many many base pairs. Your quotation of Terry’s definition and Peter’s interpretation is spot on, but the crucial word is functional. When we get to functional units we have to address exons and introns which I will  not go into now, suffice to say that a functional unit of a gene codes for specific proteins and enzymes, which may be changed by different modifiers and mutations.
                                        Due to the complexity of gene structure, different segments of a gene may mutate, giving origin to different alleles which may appear (act) like another gene, in which case we talk of heteroalleles. When the same functional unit is involved, we get homoallelic relations.
                                         
                                        The control of psittacins in toto must be a massive task for one or two genes, with very little research results available on commercially-directed studies on poultry as an example. We must assume that more than one gene, or many, may be involved, given the complexity of psittacin production that must be in place, and that these genes may be massive in size, with many functional segments but still forming part on a specified gene. Read the first sentence again.
                                         
                                        If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele? How will this then be proven?
                                         
                                        I believe that the expression of the normal wildtype allele is the normal state and not an additional expense of energy, therefore mutations at these loci are inhibitory in nature and the homozygote appears closer to the normal wildtype phenotype, unless we have a situation where the homozygotic form appears closer to the complete mutation than the heterozygote, that we see in other spp. But in this latter instance we must not overlook epistasis in the heterozygote, where one gene could code for a protein preventing transcription of the other gene. Also, epistasis must be differentiated from dominance at the homoallelic level that points to an interaction between alleles at the same gene functional unit. And not the least, intragenic complementation but this must refer to heteroalleles which is not applicable here, it refers to two alleles complementing in the heteroallelic event; we are referring to a homoallelic difference, unless we have an unexpected situation of heteroalleles, other than in the ringneck. These 3 functional options may all explain the phenomenon where the homozygote appears closer to the complete mutation allele than the heterozygote.
                                         
                                        Deon
                                         
                                         
                                         
                                         
                                         
                                         
                                        Sent: Saturday, August 04, 2012 8:54 PM
                                        Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                         
                                         
                                        Hi Deon,
                                         
                                        I adept completely to the phylosophical part (even and specially to the criteria of begining of life) ... but this forum is about a different subject.
                                         
                                        A homozygotic parblue can never be phenotypically wild-type. Are you sure? Remember what you have just written : We live in a changing world and so we have to adapt and start thinking about the inadequacies of established systems and start formulating new criteria and new directions of thinking, considering what we know today and what we believe we know.
                                        I think that it depends whether this parblue acts through an inhibitory mechanism (then you would be rigth) or through an activatory mechanism (then your sentence would not be correct). Imagine a parblue mutation able to decrease the final psittacine of 40% (it means that 60% of the psittacine is expressed) when only one allele of this parblue is expressed (Ex ParblueBlue).
                                         
                                        1. If activatory mechanism :
                                        WildParblue ..... wild phenotype
                                        ParblueBlue ..... parblue phenotype (psittacine expression of 60% since there is only an activation of 60% of the system leading to psittacin production)
                                        ParblueParblue ..... wild phenotype since the theoretical capacity of psittacine production is 120% (60% from each Parblue allele) .... wild phenotype.
                                         
                                        2. If inhibitory mechanism:
                                        WildParblue ..... wild phenotype.
                                        ParblueBlue ..... parblue phenotype (psittacine expression of 60% since there is a block of 40% in the capacity of the metabolic path leading to psittacin production due to the increase in the production of an inhibitory agent).
                                        ParblueParblue ..... parblue phenotype expressing only 20%. The homozygous form of the Parblue only expresses 20% since each Parblue allele blocks 40% of the expression. This is a bluish phenotype.
                                         
                                        So, for a Parblue mutation able to express more than 50% of the final product when it is present in the heterozygous form (BlueParblue) and acting through an activatory mechanism, it would be posible to get an apparent wild phenotype in the homozygous form (ParblueParblue). Please, if you think that I am wrong .... could you tell me specifically why/where in my reasoning?
                                         
                                        Why everybody accepts the same reasoning for an activatory mechanism if the parblue mutation expresses less than 50% of the final product (let's say 30%) in the heterozygous form, so that in the homozygous form (60% of psittacin expression) we get a greener bird with less than 100% expression, that is a heavy parblue? Is this reasoning valid only when it conforts our previous ideas? Let's open our minds ... and if I am wrong ... let me know it .... with reasons.
                                         
                                        Maybe the problem is that you are thinking that the mutated genes are the same for both mechanisms ... but this is wrong : only in the activatory mechanism we can properly speak of parblues because the partially mutated gene is the same which completely blocks psittacin production (Blue). In the inhibitory mechanism the mutated gene is different. It is coding for a different enzyme, acting by an inhibitory mechanism in psittacine synthesis ... and this is the reason that I said that we can not compare two apparent parblues mutations in different species when the homozygous parblues behave differently (greener in one specie and bluer in the other).
                                         
                                        Even with 80% psittacin retention in a homoallelic homozygous event, there is still a 20% loss of...exactly what? Quantitative decrease of psittacins as a collective homogenous mass of different psittacins? What about the quality, where are the control points for facets of psittacins; colour tone, brilliance, hue, interactions, all the possible modifications, the millions of available colour expressions.
                                         
                                        I agree ... and this is why we are here.... trying to approach the "truth", even that our models are too simple. Knowledge is like a sphere : when it increases, the number of external points touching the "unknown" also increase, and this is why the most knowledgable people are those with more doubts and questions. I am sure that some of the persons who doubt the most here are Terry and Inte ... and that this is the reason their presence is rare : we can not answer their questions ... but our questions could trigger new ideas in their minds, so they both should be a little more presents.
                                         
                                        Regards
                                         
                                        Recio
                                        From: Deon Smith <gms1@...>
                                        To: Genetics Psittacine <genetics-psittacine@yahoogroups.com>
                                        Sent: Saturday, August 4, 2012 2:51 PM
                                        Subject: Fw: [Genetics-Psittacine] Parblues IRN do not exist
                                         
                                         
                                        Sorry, correction
                                         
                                        Sent: Saturday, August 04, 2012 2:34 PM
                                        Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                         
                                         
                                        We are trying to align natural events within boundaries/divisions we have created, instead of the other way round. This all in an effort to understand things according to present knowledge.
                                        What we have seen lately, is the fading of man-made boundaries in established man-made classification systems with the advances in and release of knowledge. As an example, look at the definitions for inheritance behaviour; dominant, recessive etc. We live in a changing world and so we have to adapt and start thinking about the inadequacies of established systems and start formulating new criteria and new directions of thinking, considering what we know today and what we believe we know.
                                         
                                        Look at the man-made divisions in the development of a new life in legal definitions of when a developing new individual may be executed through legal abortion, decided on by Someone playing God that is putting up divisions in a process of programmed continuing development.
                                         
                                        A homozygotic parblue can never be phenotypically wild-type. Even with 80% psittacin retention in a homoallelic homozygous event, there is still a 20% loss of...exactly what? Quantitative decrease of psittacins as a collective homogenous mass of different psittacins? What about the quality, where are the control points for facets of psittacins; colour tone, brilliance, hue, interactions, all the possible modifications, the millions of available colour expressions. The exchange of one metal molecule for another in the white paper for colour production, brought about by a single base substitution and the major effect of such a minute alteration.
                                         
                                        Deon
                                         
                                        Sent: Saturday, August 04, 2012 12:52 PM
                                        Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                         
                                         
                                        Peter, Deon, Terry, Wynand, .... every other with knowledge in "the smart stuff",
                                         
                                        I have checked that the definitions of homoalleles and heteroalleles made by Terry are correct... but I have a problem for understanding it : it seems that the changes in nucleotide composition in one specific part of a gene will always produce a change in the quantity of the RNAm produced ... a change in the quantity of the protein produced ... a quantitatif change in the final effect we see .... but changes in a different part of the same gene will finally produce,  by a similar mechanisms, quantitatif changes in a different final effect that we see. In fact it seems that those heteroalleles act as if they were consecutive genes, but, I guess, without a stop codon. Is it the case? If it is the case ... how can we make the difference between two extremely linked genes and two heteroalleles? ... and which would be the functional differences allowing for identification of one or another?
                                         
                                        First problem : most of the proteins involved in colour regulation are enzymes. The activity of enzymes is highly dependent on its tridimensional structure, and this structure depends mainly on the disposition of some specific aminoacids (those showing an asymetric -NH3 or -COOH), hydrogen bridges, ... that is, on the repartition of electric charges. A change in just one aminoacid can completely change the tridimensional structure of the enzyme and, thus, its activity. We can have different mutations acting at the same point of the gene. Some of them will be able to induce little changes, if any, in the final expression allowing for a change in the quantitatif final effect (classical homoalleles), but others, acting on the same point could induce a big change in the spatial configuration allowing the production of a different enzyme with or without a functional activity. So the same point of the same gene could produce apparent homoalleles and heteroalleles.
                                         
                                        Second problem: In the same way I can imagine that mutations acting in different parts of the same gene, could lead to a similar final tridimensional structure of the enzyme, producing just a little change in the quantitatif production of the final effect, as if both mutations were homoallelic, despite that they are acting on different points of the same gene.
                                         
                                        So, how can we say if two alleles behave as homoalleles or as heteroalleles without genetic studies? Which are the criteria to assume one or the other?
                                         
                                        Regards
                                         
                                        Recio
                                         








                                      • Deon Smith
                                        Thanks for this info Peter, interesting information. Shows us the power of natural selection in evolution. Makes one think about the head-colour of Plumheads,
                                        Message 19 of 27 , Aug 5 9:42 AM
                                          Thanks for this info Peter, interesting information. Shows us the power of natural selection in evolution. Makes one think about the head-colour of Plumheads, Slaytyheads, all Amazons and in fact every spp.
                                           
                                          Deon
                                           
                                          Sent: Sunday, August 05, 2012 4:47 PM
                                          Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                           
                                           

                                          Hi Guys,
                                           
                                          I would reffer to the Gouldian finch. There are three headcolors in the wild. Redhead, Blackhead and Orange. Long it was thought that the Blackhead Gould(recessive sexlinked) was the original wildtype because of his majority. Today it is generally accepted that the Redhead(Dominant sexlinked) was the original wildtype. This is an example where a mutation replaces the wildtype, but I’m not sure whether they are on the same locus.
                                           
                                          Regards
                                          Peter 
                                           
                                          Sent: Sunday, August 05, 2012 3:48 PM
                                          Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                           
                                           

                                          Recio said:  ...the concept of wild allele should be changed by the concept of "prevalent" allele in a given population.
                                           
                                          This is technically correct but what reality examples do you have of this? Terry mentioned in his last postings the situation where a mutation actually replaced the wild-type, I think it was an Opaline Stella or something, but this was in a captive environment. The concept of wild-type will remain valid ad infinitum, you must be careful not to confuse people!
                                           
                                          I get the idea you want to promote, but it is a pity you could not use Lutino, a simple single mutation instead of a combo type but your idea is sound and I am glad to say a perfect demonstration of my philosophical remarks about new trends in thinking and an open mind, new perceptions, not taking existing perceptions as holy cows.
                                           
                                          I believe wild-type will remain the reference standard forever, do you foresee anything else replacing it in the next 100000 years?
                                           
                                          Deon
                                           
                                          Sent: Sunday, August 05, 2012 2:29 PM
                                          Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                           
                                           

                                          Hi Deon,
                                           
                                          You have explained some of the possibilities to explain results at the genetic level. You could even add transformations of the initially produced protein so that it is sliced in different proteins with different functions, even that they come all of them from the same gene (Ex: proopiomelanocortin producing several hormones and peptides : http://en.wikipedia.org/wiki/Proopiomelanocortin) ... but the question remains intact :
                                           
                                          If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele?
                                           
                                          I will tell you a history so you will understand that wild alleles do not "exist" (as well as mutated alleles) :
                                          Recio was a selfconfident man leaving in Whiteland. In Whiteland every animal was white because of the white environement due to snow : there were white rabbits, white mice, .... and wild IRNs with a white phenotype and black eyes who had wonderfully adapted to the environement centuries ago. From men memory these birds had always been there, and they were even represented in the oldest totems that archeologist have found. Recio detected that from time to time there were spontanous mutations in the white wild IRN producing strange birds who were called dom pied IRN, since the mutation acted as dominant and the birds showed a patched expression of melanin. Some bird breeders in Whiteland had even proven that whenever two heterozygous birds were paired, they could get a strange mutant showing a green phenotype. Thus the homozygous form of the dom pied mutation was called green mutant.
                                          At the time the first green mutant was detected Recio contacted his friend Deon who was living in a warm country and was also a bird hobby man. He sent to him some pics of the wild bird (white phenotype), the heterozygous bird (dom pied) and the homozygous bird (green mutant) telling to Deon that this strange mutation behaves as incomplete dominant. When Deon received the pics with the labelled mutations, he was sure that Recio had made a mistake when labeling the pics, because in his country the wild bird was green and the homozygous mutation was white.
                                           
                                          Tell me my friends ... who of both Recio or Deon was right? Were both right? This is my feeling .... and if both of them were right it means that the concept of wild allele should be changed by the concept of "prevalent" allele in a given population. If the different alleles of a gene are considered in a "democratic" way, with all of them having the same "importance", we will accpet easierly that what can happen to one of them, can happen to any other. Thus our initial question ....
                                           
                                          If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele?
                                           
                                          .... could be reformuleted as follows:
                                           
                                          If a homozygous homoallelic event appears phenotypically identical to the mutant type, does it represent an allele at all, different to the mutant-type allele?
                                           
                                          We have changed wild by mutant (which in fact is the same as we have seen) and now it seems easier to reformulate the question as : could we get the same phenotypic expression from two different homozygous mutant alleles?
                                           
                                          What's you feeling?
                                           
                                          Recio
                                           
                                          From: Deon Smith <gms1@...>
                                          To: Genetics-Psittacine@yahoogroups.com
                                          Sent: Sunday, August 5, 2012 12:40 AM
                                          Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                           
                                           
                                          To get back to basics: a gene is a functional unit of heredity. It is a segment of DNA that is responsible for the physical and inheritable characteristics or phenotype of a living organism.A gene is made up of sequences of base pairs of variable length, where each base pair may potentially be subject to mutation; each base pair being physically able to have 3 different alleles of forms, apart from the wild type allele. But a gene may span many many base pairs. Your quotation of Terry’s definition and Peter’s interpretation is spot on, but the crucial word is functional. When we get to functional units we have to address exons and introns which I will  not go into now, suffice to say that a functional unit of a gene codes for specific proteins and enzymes, which may be changed by different modifiers and mutations.
                                          Due to the complexity of gene structure, different segments of a gene may mutate, giving origin to different alleles which may appear (act) like another gene, in which case we talk of heteroalleles. When the same functional unit is involved, we get homoallelic relations.
                                           
                                          The control of psittacins in toto must be a massive task for one or two genes, with very little research results available on commercially-directed studies on poultry as an example. We must assume that more than one gene, or many, may be involved, given the complexity of psittacin production that must be in place, and that these genes may be massive in size, with many functional segments but still forming part on a specified gene. Read the first sentence again.
                                           
                                          If a homozygous homoallelic event appears phenotypically identical to the wild-type, does it represent an allele at all, different to the (normal) wild-type allele? How will this then be proven?
                                           
                                          I believe that the expression of the normal wildtype allele is the normal state and not an additional expense of energy, therefore mutations at these loci are inhibitory in nature and the homozygote appears closer to the normal wildtype phenotype, unless we have a situation where the homozygotic form appears closer to the complete mutation than the heterozygote, that we see in other spp. But in this latter instance we must not overlook epistasis in the heterozygote, where one gene could code for a protein preventing transcription of the other gene. Also, epistasis must be differentiated from dominance at the homoallelic level that points to an interaction between alleles at the same gene functional unit. And not the least, intragenic complementation but this must refer to heteroalleles which is not applicable here, it refers to two alleles complementing in the heteroallelic event; we are referring to a homoallelic difference, unless we have an unexpected situation of heteroalleles, other than in the ringneck. These 3 functional options may all explain the phenomenon where the homozygote appears closer to the complete mutation allele than the heterozygote.
                                           
                                          Deon
                                           
                                           
                                           
                                           
                                           
                                           
                                          Sent: Saturday, August 04, 2012 8:54 PM
                                          Subject: Re: [Genetics-Psittacine] Parblues IRN do not exist
                                           
                                           
                                          Hi Deon,
                                           
                                          I adept completely to the phylosophical part (even and specially to the criteria of begining of life) ... but this forum is about a different subject.
                                           
                                          A homozygotic parblue can never be phenotypically wild-type. Are you sure? Remember what you have just written : We live in a changing world and so we have to adapt and start thinking about the inadequacies of established systems and start formulating new criteria and new directions of thinking, considering what we know today and what we believe we know.
                                          I think that it depends whether this parblue acts through an inhibitory mechanism (then you would be rigth) or through an activatory mechanism (then your sentence would not be correct). Imagine a parblue mutation able to decrease the final psittacine of 40% (it means that 60% of the psittacine is expressed) when only one allele of this parblue is expressed (Ex ParblueBlue).
                                           
                                          1. If activatory mechanism :
                                          WildParblue ..... wild phenotype
                                          ParblueBlue ..... parblue phenotype (psittacine expression of 60% since there is only an activation of 60% of the system leading to psittacin production)
                                          ParblueParblue ..... wild phenotype since the theoretical capacity of psittacine production is 120% (60% from each Parblue allele) .... wild phenotype.
                                           
                                          2. If inhibitory mechanism:
                                          WildParblue ..... wild phenotype.
                                          ParblueBlue ..... parblue phenotype (psittacine expression of 60% since there is a block of 40% in the capacity of the metabolic path leading to psittacin production due to the increase in the production of an inhibitory agent).
                                          ParblueParblue ..... parblue phenotype expressing only 20%. The homozygous form of the Parblue only expresses 20% since each Parblue allele blocks 40% of the expression. This is a bluish phenotype.
                                           
                                          So, for a Parblue mutation able to express more than 50% of the final product when it is present in the heterozygous form (BlueParblue) and acting through an activatory mechanism, it would be posible to get an apparent wild phenotype in the homozygous form (ParblueParblue). Please, if you think that I am wrong .... could you tell me specifically why/where in my reasoning?
                                           
                                          Why everybody accepts the same reasoning for an activatory mechanism if the parblue mutation expresses less than 50% of the final product (let's say 30%) in the heterozygous form, so that in the homozygous form (60% of psittacin expression) we get a greener bird with less than 100% expression, that is a heavy parblue? Is this reasoning valid only when it conforts our previous ideas? Let's open our minds ... and if I am wrong ... let me know it .... with reasons.
                                           
                                          Maybe the problem is that you are thinking that the mutated genes are the same for both mechanisms ... but this is wrong : only in the activatory mechanism we can properly speak of parblues because the partially mutated gene is the same which completely blocks psittacin production (Blue). In the inhibitory mechanism the mutated gene is different. It is coding for a different enzyme, acting by an inhibitory mechanism in psittacine synthesis ... and this is the reason that I said that we can not compare two apparent parblues mutations in different species when the homozygous parblues behave differently (greener in one specie and bluer in the other).
                                           
                                          Even with 80% psittacin retention in a homoallelic homozygous event, there is still a 20% loss of...exactly what? Quantitative decrease of psittacins as a collective homogenous mass of different psittacins? What about the quality, where are the control points for facets of psittacins; colour tone, brilliance, hue, interactions, all the possible modifications, the millions of available colour expressions.
                                           
                                          I agree ... and this is why we are here.... trying to approach the "truth", even that our models are too simple. Knowledge is like a sphere : when it increases, the number of external points touching the "unknown" also increase, and this is why the most knowledgable people are those with more doubts and questions. I am sure that some of the persons who doubt the most here are Terry and Inte ... and that this is the reason their presence is rare : we can not answer their questions ... but our questions could trigger new ideas in their minds, so they both should be a little more presents.
                                           
                                          Regards
                                           
                                          Recio
                                          From: Deon Smith <gms1@...>