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Re: [Genetics-Psittacine] Dominant - Recessive

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  • Recio Joaquin
    Hi everybody,   I will develop the idea in the days to come. Rigth now I am pretty busy and lacking of time. Regards   Recio ________________________________
    Message 1 of 34 , Nov 3, 2012
      Hi everybody,
       
      I will develop the idea in the days to come. Rigth now I am pretty busy and lacking of time.
      Regards
       
      Recio


      From: Deon Smith <gms1@...>
      To: Genetics Psittacine <genetics-psittacine@yahoogroups.com>
      Sent: Wednesday, October 31, 2012 5:45 PM
      Subject: [Genetics-Psittacine] Dominant - Recessive
       
      Recio
       
      You remarked:
       
      What I am proposing is a general rule for many supposed recessive mutations in which some split birds can be identified, and which could be treated as incomplete dominant with a variable degree of penetrance of the heterozygous form (split birds).
       
      What mutations do you see as such?
       
      Deon
    • Recio Joaquin
      Hi Marc,   The Hardy-Weinberg principle treats about the constancy of the frequency of alleles in a closed population. It was explained by Terry in an old
      Message 34 of 34 , Nov 15, 2012
        Hi Marc,
         
        The Hardy-Weinberg principle treats about the constancy of the frequency of alleles in a closed population. It was explained by Terry in an old post. You know it perfectly and you know that it is only a theoretical model.
         
        From Wikipedia :
        The Hardy–Weinberg principle (also known by a variety of names: HWP, Hardy–Weinberg equilibrium model, HWE, Hardy–Weinberg Theorem, or Hardy–Weinberg law) states that both allele and genotype frequencies in a population remain constant—that is, they are in equilibrium—from generation to generation unless specific disturbing influences are introduced. Those disturbing influences include non-random mating, mutations, selection, random genetic drift, gene flow and meiotic drive. It is important to understand that in real populations, one or more of these "disturbing influences" are always in effect. That is, Hardy–Weinberg equilibrium is an ideal state that provides a baseline against which change can be analyzed.
        Static allele frequencies in a population across generations assume: no mutation (the alleles don't change), no migration or emigration (no exchange of alleles between populations), infinite population size, and no selective pressure for or against any genotypes.
         
        I have not made any work on allele frequencies/speciation. I have just used an example trying to pass an idea. That's all.
         
        This forum is to discuss ideas and to test them. Rigth now the hypothesis of Emeradl as an independent incomplete dominant non parblue mutation is being checked in IRN and Alex. Similar for the hypothesis of Deep as a possible melanistic mutation and for the possibility of Grey as a possible incomplete dominant mutation. As I wrote recently to Lee this is the power of this forum : one person owns the bird, another can recognise the specific mutation, a third one will do the test breeding and another the ultraviolet studies, ... and finally Deon, Terry, Wynand and others will put all the findings in the theoric framework and print it for the posterity (and for us, of course).
        Who could be a better reviewer than the people in this list?
        How could the ideas be shared more quickly than in this forum?
        Where, other than here, would you meet people more interested in this subject?
        How could people acces to birds which do not exist in their countries? I have been writing a lot about Emeralds ... but I have never seen an Emerald bird in the flesh. How could I have written about it if I was not in this forum, with the input of all other breeders? ... and you say that this forum has no credibility? But it is here where the new mutations are presented and ideas are "popping up".
         
        Do not think that the ideas come into the mind as a miracle. They are induced by the input of everybody here. Johan and Tienie are the "inductors" of the hypothesis of the apparent expression of an heterozygous recessive mutation when it is combined with another mutation. Madas was the "inductor" of Grey as a possible incomplete dominat mutation, ... and so on. I am feeeding on others comments as, I hope, others are feeding on my comments; and if I can contribute in any way to a better understanding ... that is enough for me. Twenty years ago I was publishing "science" and I can assure you that I prefere the exchange of ideas in this forum than the exchange of letters with a reviewer to obtain the "permission" to publish without knocking over his ideas.
         
        Why are you always doing the same type of comments instead of contributing to the list with the research you are leading?
         
        Regards
         
        Recio
        From: docnoakes16 <marc.noakes@...>
        To: Genetics-Psittacine@yahoogroups.com
        Sent: Thursday, November 15, 2012 8:33 PM
        Subject: [Genetics-Psittacine] Re: Dominant - Recessive
         
        Recio - your stories and anecdotes attempt to engage people and help them understand the mechanisms of inheritance, and I applaud you for that. However, my two greatest fears are that your "hypothesese" will remain pure banter on a web forum (which has no credibility) until someone provides data for validation, and also that many ideas are being accepted here without first being tested.

        We really MUST start doing this properly. Its a great shame that your work is not being recognised in the scientific community....and let's face it....what you are writing on this site IS science! The same thing happened to Mendel...if you remember.

        Lastly, can you comment on how Hardy-Weinberg fits in with your work on allele frequencies and speciation in your story.

        Best
        Marc

        --- In mailto:Genetics-Psittacine%40yahoogroups.com, Allan Macdonald <asplandbird@...> wrote:
        >
        > what happened to the grey females
        >
        >
        >  
        > Allan Macdonald <asplandbird@...>
        >
        >
        > ________________________________
        > From: Recio Joaquin <jrecio99@...>
        > To: "mailto:Genetics-Psittacine%40yahoogroups.com" <mailto:Genetics-Psittacine%40yahoogroups.com>
        > Sent: Wednesday, 14 November 2012 7:58 PM
        > Subject: Re: [Genetics-Psittacine] Dominant - Recessive
        >
        >
        >  
        > ... and let's finish
        the whole story:
        >  
        > The great, great, ... great grandson decided to keep some birds for breeding. At that time it was clear for him that the former birds had evolved and produced two distinct species. These new species were named "whitish" and "reddish" according to the first descriptions where only the male colour was the distinct feature. He did not have enough place in his aviaries and decided to keep only the smaller birds (reddish). He offered the whitish birds to a friend living in the mountains and owing big aviaries.
        >  
        > Time passed and 10 years later a white bird appear among his reddish. It was like all the other reddish in size, behaviour, feeding, ... but white. He was excited and phoned to his friend in the mountains, just to know that among his friend's whitish birds 2 red birds had also appeared, keeping all the other featues of the whittish species. They decided to test breed both mutants
        and they found that the white mutant showed a pure recessive behaviour respective to the "reddish" and that the red mutant showed a pure dominant behaviour respective to the "whitish". Since the inheritance pattern of both mutations were completely different they concluded that they were both different mutations appearing in different species ...
        >  
        > ... and you ... which is your conclusion?
        >  
        > This story ends here.
        >  
        > Regards
        >  
        > Recio
        >
        > From: Recio Joaquin <jrecio99@...>
        > To: "mailto:Genetics-Psittacine%40yahoogroups.com" <
        ymailto="mailto:Genetics-Psittacine%40yahoogroups.com">mailto:Genetics-Psittacine%40yahoogroups.com>
        > Sent: Tuesday, November 13, 2012 8:38 PM
        > Subject: Re: [Genetics-Psittacine] Dominant - Recessive
        >
        >  
        > Let's continue;
        >  
        > At that time no one could help those brave breeders, just like now.
        >  
        > Five centuries passed before the great, great, ... great grandson of one of the first spanish breeders find the note book of his great, great, ... great grandfather. He was also a bird breeder and, luckily the spanish economic crisis was over and he had enough money to go back to the "strange country". He took the pics and the notebooks of the first and second expeditions and went to verify by himseld what his ancestors had described.
        >  
        > He found in the upper northern mountains some white males : they were bonny birds, bigger than those
        described in the old notebooks, with powerfull wings. Even the females were bigger and ligther. When studing their behaviour he noticed that, although they were always omnivorous, they have become reputable killers of mice and other little mammals.
        >  
        > In the lower parts of the southern mountains he could not find any red bird. Local people told him to enter in the iron mines to look for them. He did so and he could find the red birds ... but they were different : they were smaller than described in previous reports, ... and darker, even the females, ... and with big eyes. They had become very shy and he only went out of the mines during the nigth for eating some berries and insects. They did not like to fly and had become very good runners.
        >  
        > He was as puzzled as his ancestors but he was a proud man and he decided to prove definitely which was the inheritance
        pattern of those birds. He took some birds of both types to cross breed ... but he could only produce some sterile hybrids.
        >  
        > Anyone could help this amazed breeder?
        >  
        > Regards
        >  
        > Recio
        >
        > From: Recio Joaquin <jrecio99@...>
        > To: "mailto:Genetics-Psittacine%40yahoogroups.com" <mailto:Genetics-Psittacine%40yahoogroups.com>
        > Sent: Monday, November 12, 2012 7:34 PM
        > Subject: Re: [Genetics-Psittacine] Dominant - Recessive
        >
        >  
        > Let's continue,
        >  
        > Spanish breeders did a good job and could stablish without any doubt that
        the mutation inherited through the autosomes, but it was only visible in males because its expression was dependent on the presence of testosterone, and thus the females remained grey. Nevertheless the question of which one was the wild bird and which one was the mutated bird was always open, as well as the inheritance pattern (pure dominant or pure recessive) since the breeding data for one and for the other were extremely correct.
        >  
        > This question and its economics issues became so important that an international team was formed for the second expedition. Australians and Southafrican breeders (the best at that moment in this familly bird) were recruted and they went to the "strange country". Reliable local sources told them that numerous birds had been seen in the mountains, and both teams spent 2 weeks trapping birds before coming back to Spain. The Australian team was trapping birds in the upper northern
        part of the mountains, full of snow, and they could trap 95% of white males and only 5% of red males. The Southafrican team was trapping birds in the lower southern part of the mountains, full of iron mines, and they got 95% of red males and only 5% of white males.
        >  
        > The expedition came back to Spain with the birds and the results were exposed. No one spanish breeder went to the strange country because of his chronic economic crisis, and after hearing the results they were all puzzled. They did not yet have the answer : which one was the wild and which one was the mutated bird? which is the real inheritance pattern?
        >  
        > Could you please help them?
        >  
        > Regards
        >  
        > Recio
        >
        > From: Allan Macdonald <asplandbird@...>
        > To: "
        ymailto="mailto:Genetics-Psittacine%40yahoogroups.com">mailto:Genetics-Psittacine%40yahoogroups.com" <mailto:Genetics-Psittacine%40yahoogroups.com>
        > Sent: Monday, November 12, 2012 3:36 PM
        > Subject: Re: [Genetics-Psittacine] Dominant - Recessive
        >
        >  
        > Would depend on whether you prefer red or white and where does grey fit into the senario (plenty grey females easier to trap) perhaps they are both right and the wild type colour is grey
        >
        >  
        > Allan Macdonald <asplandbird@...>
        >
        > From: Recio Joaquin <jrecio99@...>
        > To: "mailto:Genetics-Psittacine%40yahoogroups.com"
        <mailto:Genetics-Psittacine%40yahoogroups.com>
        > Sent: Monday, 12 November 2012 8:43 PM
        > Subject: Re: [Genetics-Psittacine] Dominant - Recessive
        >
        >  
        > Hi,
        >  
        > I will give you a clue :
        >  
        > There was an spanish expedition to an strange country where an unknown very scarce bird was discovered. It was so rare that only two young males were traped : their colour was grey but becoming adult one of them became red and the other one became white. There were plenty of grey females (easier to trap) and both males were paired to the grey females. Looking at the breeding results one of the trappers said that his bird (red one) was a new mutation and that it inherited as pure dominant, the other white
        male being the wild male phenotype. But the trapper owing the white male said that his breeding results proved that his bird (the white one) was a new albinistic mutation with a pure recessive behaviour respective to the red one which was in fact the wild type. Breeders were ready to pay a lot of money for the mutated birds, but not as much for the wild birds since a new expedition to the strange country was ready to start, and more wild birds will
        > arrive.
        >  
        > Who was rigth? For which bird would you pay thousands dollars?
        >  
        > Come on, do not be shy ...
        >  
        > Recio
        >
        > From: Recio Joaquin <jrecio99@...>
        > To: "mailto:Genetics-Psittacine%40yahoogroups.com" <
        rel=nofollow target=_blank ymailto="mailto:Genetics-Psittacine%40yahoogroups.com">mailto:Genetics-Psittacine%40yahoogroups.com>
        > Sent: Sunday, November 11, 2012 3:48 PM
        > Subject: Re: [Genetics-Psittacine] Dominant - Recessive
        >
        >  
        > Really expecting comments ... but there are no comments ... it means that everything is clear..... mmmhhh!!!
        >  
        > Little question to verify : do you think that the number of pure dominant mutations/alleles is higher, lower, similar or eaqual than the number of pure recessive mutations/alleles?
        >  
        > Regards
        >  
        > Bored Recio with too much free time ... today.
        >
        >
        > From: Recio Joaquin <jrecio99@...>
        > To: "
        ymailto="mailto:Genetics-Psittacine%40yahoogroups.com">mailto:Genetics-Psittacine%40yahoogroups.com" <mailto:Genetics-Psittacine%40yahoogroups.com>
        > Sent: Saturday, November 10, 2012 1:33 PM
        > Subject: Re: [Genetics-Psittacine] Dominant - Recessive
        >
        >  
        > Hi everybody, let's continue.
        >  
        > One of the aims of the genetic list is to identify the same mutations among different species and to uniform nomenclature. One of the criterion to identify the same mutation is the inheritance mode. This inheritance mode is perceived as something of static and permanent through different species, but this is not the case. We should remember that the genetic make up of the species we see now is the result of millions years of mutation and selection, and
        that we should consider every species as the present mixture of the most prevalent alleles. What we call "wild" alleles are exactly the same that the "mutated" alleles and they can behave as recessive, dominant or "intermedial" (incomplete dominant = incomplete recessive).
        >  
        > If we consider that the genetic make up of a species is the present mixture of the most prevalent alleles, and that we know that the genetic control of pigments synthesis depends on many genes, we can understand that the final amount of pigment production (melanin or psittacofulvines) is species specific. We have just seen that the expression of a mutation (visual phenotype for our eyes) depends where in the sigmoide curve this mutation is acting, and this point depends of the final amount of pigment produced by each species. This is species specific and when considering the action of any mutation we should also consider where in
        the curve the final amount of pigment is located for that specific species.
        >  
        > The same mutation (incomplete dominant) can act in a species in the upper part of the curve and appear as recessive to our eyes (acting on point A), and it could act at a lower point (C) in other species and appear as incomplete dominant with low expressivity or partial penetrance, or even at a lower point (in the middle of the curve) and appear as incomplete dominant. I am not saying that the mutation behaves differently. The mutation always acts in the same way in every species but our "device" to detect it (our eyes) does not allow to detect it in all conditions. The same % decrease in pigment concentration induced by a mutation will be detected by our eyes as recessive, incomplete dominant with low expressivity/penetrance or as incomplete dominant depending on which species this mutation is acting, that is depending on how much pigment the "wild"
        bird owns.
        >  
        > In most birds the amount of pigment is similar because they are exposed to similar environemental presion and we can always keep our "way of working", but when considering mutations placed at the limit points of detection (points B and C) we should keep in mind that its phenotypical expression (to our eyes) in heterozygous mutations can vary from one species to another. These mutations are characterized by owing some detectable split birds (ADM pieds, opalines, ...) and/or by changing its apparent inheritance behaviour when combined to other mutations inducing a transfer to a lower point in the sigmoide curve.
        >  
        > Probably most of the mutations inherit asincomplete dominant and thus these considerations should be kept in mind. For "pure" dominant or recessive mutations these ideas are useless ... but we do not have any confident tool to know for sure that we are dealing with these pure
        dominant or recessive mutations.
        >  
        > In IRN the only mutation that could be considered as pure dominant is Grey. To be further sure that it is dominant we should produce SF and DF grey diluted birds. If their phenotype is the same very probably grey should be considered as dominant, but if their phenotype is different it will prove that Grey is also an incomplete dominant mutation, like Dark or Violet.
        > This method would allow for "fine tuning" in the determination of the inheritance pattern of each mutation, and every apparent pure dominant or recessive mutation should be studied in combination with another mutation allowing to uncover a possible "hidden" incomplete dominant behaviour. Maybe Peter is rigth and all the mutations are, in fact, incomplete dominant (or incomplete recessive ... just a nomenclature game).
        >  
        > Really expecting comments.
        >  
        > Regards
        >  
        >
        Recio
        >  
        >
        >
        > From: Recio Joaquin <jrecio99@...>
        > To: "mailto:Genetics-Psittacine%40yahoogroups.com" <mailto:Genetics-Psittacine%40yahoogroups.com>
        > Sent: Friday, November 9, 2012 8:44 PM
        > Subject: Fw: [Genetics-Psittacine] Dominant - Recessive
        >
        >  
        > Addendum:
        >  
        > Many IRN breeders are working on the interaction between Deep, Dark and Violet in the blue series. All of them seem to behave as incomplete dominant mutations and the number of possible combinations considering SF and DF possibilities is very high. Honestly I am not able at all
        to make the difference among many of them. A similar situation raises when considering some mutations as Grey, Slaty, Kaki or Dhani in green series birds.
        >  
        > All these mutations have a common point : they are dealing with high intensity colour perception.
        >  
        > I understand that the raise is to get the darker or more purple bird, but if we really want to understand how each mutation can affect the expression of the others, we should work by combining these mutations in the middle point of the sigmoid curve, by adding a diluting mutation (citron or dilute). In this way our area of colour perception will be expanded, and we will not need to inverse colours or to work with photoshop to detect minimal changes in colour expression.
        >  
        > Regards
        >  
        > Recio
        >  
        >
        >
        > From: Recio Joaquin <jrecio99@...>
        > To: "
        href="mailto:Genetics-Psittacine%40yahoogroups.com" rel=nofollow target=_blank ymailto="mailto:Genetics-Psittacine%40yahoogroups.com">mailto:Genetics-Psittacine%40yahoogroups.com" <mailto:Genetics-Psittacine%40yahoogroups.com>
        > Sent: Friday, November 9, 2012 2:39 PM
        > Subject: Re: [Genetics-Psittacine] Dominant - Recessive
        >
        >  
        >
        >
        > Hi Peter,
        >  
        > Thank you for answering.
        >  
        > I was treating pigment perception and inheritance mode but we could also refer to pied mutations. In this case we should consider the colour intensity as the total % of colour lost, independtly of the effect on single feathers, and the pigment concentration should be changed by something like "migratory factors"
        concentration, which is directly related to the final amount of pigment production, and thus, of pigment concentration.
        >  
        > Let's consider the dom pied mutation in IRN : in this case we have 3 different phenotypes when considering the alleles at work:
        > The homozygous wild bird
        > The heterozygous mutant (classical harlequin)
        > The homozygous mutant (clear bird).
        >  
        > It is clear that the bird showing the highest variability in its expression is the heterozygous mutant, and we could speculate that this is the case because it is placed at mid-way in the sigmoid curve making the relation between colour intensity and "migratory factors" concentration. Very little changes in migration factors concentration at this point induce a very important change in colour intensity. The homozygous wild and mutant are placed at the extremes of the curve and even with the
        same variation in pigment concentration they show very little variability in their colour expression. What I want to outline is that mutations being expressed at the middle point of the curve will show a higher variability in its expression than mutations being expressed at the lowwer or at the upper parts. Those "middle curve" expressing mutations are more likely to produce specific strains since we can detect and select little changes in its phenotype. When I
        > speak of "mutations being expressed at the middle point of the curve" I am refering to the expression and not to the inheritance mode. Ex. the expected visible variability would be similar for an heterozygous dom pied than for an homozygous rec pied. This idea is a general rule and not only for pied mutations.
        >  
        > The same considerations can be adapted to parblues : we should expect a higher variability in the expression of Indigo or of Ligth Turquoise (both in
        the middle of the curve) morphotypes than in the expression of Saphire or Heavy Turquoise morphotypes (each at an extreme of the curve) ... and probably the parblue included in the genetic make up of saddlebacks is an specific strain of one of the formers.
        >  
        > In the attached file you can clearly notice that the visible colour change of equal changes in pigment concentration (0.5 log units in the exemple) can be indetectable to the human eye (change between -4.5 and -4 log units), slightly detectable (change between -7.5 and -7 log units) or readily visible even for "blind" people (change between -6 and -5.5 log units).
        >  
        > Now we have the background knowledge to try to understand ligth and dark phase mutants. What I am going to expose is just a possible explanation, but there are many other possibilities.
        >  
        > When do we say that a mutation shows 2 "phases"? When
        we first see the same mutation in two different intensities of colour, the first idea is that one of them is a combo of the mutation we are dealing with and a diluting or a melanistic mutation. The problem is that when we try to isolate this mutation present in the combo we can never get it. There are two possible explanations:
        > 1. Both mutations are very highly linked acting like one single mutation.
        > 2. The accompaying mutation (some people call them modifying factors) induces a very low change in pigment concentration, only visible to our eyes when this mutation acts on a pigment concentration in the middle of the sigmoid curve. When this accompanying mutation is "transfered" to the wild birds the induced change in pigment concentration is not enough to be detected by our eyes because the new mutation has been positioned on the upper part of the sigmoide curve.
        >  
        > If the second
        possibility was the rigth one ... what could we do to make "reappear" this mutation to our eyes? The easy way is to transfer the mutation to a bird already dysplaying a different mutation expressed in the middle part of the sigmoid curve. Exemple for easier understanding : we all know the existence of light and dark phase pallids. If the accompanying mutation in pallids acts slightly on melanin production we could try to transfer it to mutations expressed in the middle part of the sigmoid curve (clearhead fallows or cleartails or dilutes, ...) and we will be able to get light and dark phase clearheads fallows, cleartails, dilutes, ...
        >  
        > Comments before attacking a holly cow saying: "The same mutation inherits in the same way in every species".
        >  
        > Regards
        >  
        > Recio
        >  
        >  
        >
        > From: Peter Wouters <wouterscalant@...>
        > To:
        href="mailto:Genetics-Psittacine%40yahoogroups.com" rel=nofollow target=_blank ymailto="mailto:Genetics-Psittacine%40yahoogroups.com">mailto:Genetics-Psittacine%40yahoogroups.com
        > Sent: Friday, November 9, 2012 6:29 AM
        > Subject: Re: [Genetics-Psittacine] Dominant - Recessive
        >
        >  
        > Hi Recio,
        >  
        > There is a third possibility: we know that in several recessive mutations some split birds can be identified (ex: ADM pieds). We could consider that these mutations behave as incomplete dominant with a variable expression or penetrance of the mutation. If the production of pigment by the heterozygous bird is in C we will be able to detect 50% of split birds (those with a lower colour intensity, but not those with a higher than 95% colour intensity). When the considered production of pigment changes from C to the upper part of the curve we will find less and less detectable split birds, their %
        depending on the degree of variable expressivity of the mutation, and we will say that the penetrance of the mutation decreases.
        >  
        > I can imagine someting like this in a dillute mutation but not in a pied. A feather is pied or it isn’t. Not 95%. If I’m not mistaking pied feathers are nearly 100% pied.
        >  
        > Regards
        > Peter
        >  
        > From: Recio Joaquin
        > Sent: Thursday, November 08, 2012 11:56 PM
        > To: mailto:Genetics-Psittacine%40yahoogroups.com
        > Subject: Re: [Genetics-Psittacine] Dominant - Recessive
        >  
        >  
        > No comments ... so let's continue:
        >  
        > If you analyse the graph you will notice that the relation between colour intensity and pigment concentration is
        almost lineal only between 20 and 80% of colour intensity. In the extreme points of the graph big changes in pigment concentration do not allow significant changes in colour intensity. We are going to analyse how mutations could behave when acting on pigment concentration values in these extreme points.
        >  
        > In the attached file you will find again the saturation sigmoide curve. In the upper part you can find 3 points named A (colour intensity at 99%), B (colour intensity at 97%) and C (colour intensity at 95%, threshold for biological saturation).
        > Let's consider that A represents the colour of the wild bird. When we say that a mutation behaves as recessive what we are meaning is that our eyes can not see any difference between the wild phenotype and the heterozygous bird (split bird) and this happens in several possible situations:
        >  
        > 1. Authentic recessive behaviour : in the heterozygous bird the
        presence of one wild allele is able to keep 100% of pigment production. Both homozygous and heterozygous bird show a 99% of colour intensity (A point in both homozygous and heterozygous conditions).
        >  
        >  
        > 2. Incomplete dominant behaviour with low expressivity: in the heterozygous bird the presence of one wild allele is not able to keep 100% of pigment production. The homozygous bird shows a 99% of colour intensity (point A) and the heterozygous bird shows 97% (point B). ... but our eyes can not see the difference and we class them as recessive mutations. Do not forget that a decrease in pigment concentration of about 30% means only a change of half a log unit.
        >  
        >  
        > There is a third possibility: we know that in several recessive mutations some split birds can be identified (ex: ADM pieds). We could consider that these mutations behave as incomplete dominant with a variable
        expression or penetrance of the mutation. If the production of pigment by the heterozygous bird is in C we will be able to detect 50% of split birds (those with a lower colour intensity, but not those with a higher than 95% colour intensity). When the considered production of pigment changes from C to the upper part of the curve we will find less and less detectable split birds, their % depending on the degree of variable expressivity of the mutation, and we will say that the penetrance of the mutation decreases.
        >  
        >  
        > What we have just said for recessive mutations is also valid for dominant mutations, but with the graph translated to the opposite part of the curve when considering the heterozygous and homozygous mutant birds. Just think that a wild allele behaves as dominant respective to what we call a recessive mutation. All alleles (wild, recessive or dominants) are just alleles and when we say that one of them
        behaves as recessive respective to another, this is the same that saying that the latter behaves as dominant respective to the former. Hope it is clear.
        >  
        > I have been speaking of pigments but what it is being developped is also valid for structural mutations changing our perception of the underlying pigment (phenotypic colour).
        >  
        > Questions befor atacking the dark and ligth phase type mutations.
        >  
        > Recio
        >  
        >  
        > From: Recio Joaquin <jrecio99@...>
        > To: "mailto:Genetics-Psittacine%40yahoogroups.com" <mailto:Genetics-Psittacine%40yahoogroups.com>
        > Sent:
        Thursday, November 8, 2012 2:16 PM
        > Subject: Re: [Genetics-Psittacine] Dominant - Recessive
        >
        >  
        > Hi Deon,
        >  
        > Sorry I forgot to answer your very specific question : which mutations considered as recessive could in fact be incomplete dominant with a variable degree of expressivity and thus of penetrance? We had previously discussed this question and the candidates were ADM pieds and opaline (in IRN) and the Orangeface A. roseicollis, as proposed by Stephan. Probably there are more than these mutations, .... and very probably most of mutations classed as recessive or as dominants are, in fact, incomplete dominants.
        >  
        > I will try to develop this idea but first we need to know something about what we perceive as colour intensity and the relative amount of pigment present. In the graph below you can see that around 95% of the change in intensity colour appears on 2 log units
        (around x 100 change in concentration) of change in pigment concentration. Those are the curves we can get by measuring, with specific devices, pigment concentration and colour intensity or colour saturation.
        > Reality is more complicated since very high concentrations of pigment could be detected as a lower intensity (black line in the graph). This is just for purists and, in physiological conditions, we will not deal with such situations.
        >  
        > The graph above shows what I am explaining respective to the dilution of a pigment, but for better understanding I will express the same thing in a graph facing colour intensity to the log of pigment concentration expressed in arbitrary units. This is a graph similar to competition studies in pharmacology:
        > The percent response is the % of colour intensity and the Log [agonist] is the log [pigment]. We have seen in the first graph that the slope is around 1 (almost 95% of change
        in 2 log units). Pigment concentration increases from the left to the rigth (-9 to -3), and colour intensity increases from down (0%) to up (100% or chemical saturation).
        >  
        > What we have seen must be reinterpreted when the device to see the colour intensity is our eyes :  higher concentrations will not produce a noticeable higher intensity and lower concentrations will not be detectable.
        > In the first case (higher pigment concentration) this is due to two mechanisms : physical (pigment molecules are "hidden" behind other pigment molecules) and physiological (our cones have a maximal capacity of stimulation and higher stimuli will not produce any increase in what we see). We can call it biological saturation.
        > In the second case (lower pigment concentration) there is a threshold of detection, and below this threshold we can not detect any pigment even if a low amount is always present.
        >  
        >
        Let's say that our eye detection threshold appears at 5% of colour intensity and that our biological saturation treshold appears at 95% of colour intensity. That is we will not be able to detect any pigment producing a lower intensity than 5%, and we will not be able to "see" higher pigment concentrations than those inducing a 95% of colour intensity (biological saturation).
        >  
        > Comments before progressing, please.
        >  
        > Recio
        >  
        > From: Deon Smith <gms1@...>
        > To: Genetics Psittacine <mailto:genetics-psittacine%40yahoogroups.com>
        > Sent: Wednesday, October 31, 2012 5:45 PM
        > Subject: [Genetics-Psittacine] Dominant - Recessive
        >
        >  
        > Recio
        >  
        > You remarked:
        >
         
        > What I am proposing is a general rule for many supposed recessive mutations in which some split birds can be identified, and which could be treated as incomplete dominant with a variable degree of penetrance of the heterozygous form (split birds).
        >  
        > What mutations do you see as such?
        >  
        > Deon
        >

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