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Re: [evol-psych] The truth about RANDOM MUTATIONS.

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  • James Gray
    Edgar, I have to thank you for writing this. I have never seen Kohl admit or deny that he was a creationist. At least this gives me an idea what the random
    Message 1 of 21 , Mar 30, 2013
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      Edgar,
      I have to thank you for writing this.  I have never seen Kohl admit or deny that he was a creationist.  At least this gives me an idea what the random mutation theory is that Kohl will not describe but calls ridiculous.  However, I do not see how even a random mutation theory that worked on a passive blueprint would fail as long as the replication was reasonably good.  About 20 years ago I wrote a simulation using a dedicated computer using the language M.  It is relatively easy to write M code that can write M code.  It easy for a job running in M to spin off another job.  The only problem is that the replication is essentially perfect.  To simulate random mutation I had to have a separate reproduction module that the replicators would call to replicate themselves.  As long as the fidelity was fairly high, random mutation worked.  I did have the reproduction module make totally random errors meaning arbitrary substitution of ASCII characters.  It also randomly duplicated lines of code and randomly deleted lines of code.  There was one arbitrary non-random mutation I allowed to occur randomly.  The ability to kill competitor jobs.  To make the simulation life like I had to arbitrarily limit the life expectancy of each job.  The only resources the jobs competed for was CPU cycles and partition space.  One problem was that because of looping in software is that it was way to easy for the jobs to discover the secret to eternal life.  I did have instances where things ran for a while and then everything went extinct.

      James Gray

      On Sat, Mar 30, 2013 at 7:29 AM, Edgar Owen <edgarowen@...> wrote:
       

      All,


      As evidenced in the post below and many many others clearly most genetic changes occur via internal replicative mechanisms and NOT Kohl's "random mutation" straw man.

      But neither do they occur via what these bacteria ate or smelled as Kohl's nutty 'model' would have us believe... What an organism eats or smells does produce some minimal epigenetic changes but they DO NOT alter the genetic code.

      There are natural internal replicative mechanisms that are responsible for nearly all genetic changes. Meiosis is the most obvious, but there are many others, such as copying errors, that produce more profound changes.

      The key to understanding this is to recognize the power of DNA to produce viable organisms. Even in the face of radical changes the micro genetic machinery is highly self correcting towards producing viable organisms even in the face of considerable 'damage' some of which can be produced by random mutations. Go in and mess the DNA up and the internal mechanisms always try to patch it up so that it produces a viable organism even if that viable organism is a new organism with new genetics.

      The internal genetic machinery is not a simple passive blueprint, it is an active system that above all tries to produce a viable organism from a large repertoire of elemental building blocks, no matter if or how those building blocks have been reshuffled or even damaged.


      The 'random mutation' theory is a standard CREATIONIST (yes Kohl is a self admitted creationist) straw man that assumes DNA is a passive blueprint, rather than part of the active system I describe above. 

      Random mutations, to the extent they are responsible for genetic change, tend to work to elicit reshufflings of the basic building blocks by active internal mechanisms, rather than simply changing something in a passive fixed blueprint every bit of which must remain exact to produce a viable organism.

      Edgar



      On Mar 29, 2013, at 9:29 PM, Robert Karl Stonjek wrote:

       


      Head-on collisions between DNA-code reading machineries accelerate gene evolution

      March 29th, 2013 in Biology / Cell & Microbiology
      Head-on collisions between DNA-code reading machineries accelerate gene evolutionEnlarge

      Houra Merrikh, assistant professor of microbiology, and her student Samuel Million-Weaver, University of Washington, study mechanisms that bacteria use to evolve and adapt. Credit: Christopher Merrikh


      Bacteria appear to speed up their evolution by positioning specific genes along the route of expected traffic jams in DNA encoding. Certain genes are in prime collision paths for the moving molecular machineries that read the DNA code, as University of Washington scientists explain in this week's edition of Nature.

      The spatial-organization tactics their model organism, Bacillus subtilis, takes to evolve and adapt might be imitated in other related Gram-positive bacteria, including harmful, ever-changing germs like staph, strep, and listeria, to strengthen their virulence or cause persistent infections. The researchers think that these mechanisms for accelerating evolution may be found in other living creatures as well.

      Replication – the duplicating of the genetic code to create a new set of genes– and transcription – the copying of DNA code to produce a protein – are not separated by time or space in bacteria. Therefore, clashes between these machineries are inevitable. Replication traveling rapidly along a DNA strand can be stalled by a head-on encounter or same-direction brush with slower-moving transcription.

      The senior authors of the study, Houra Merrikh, UW assistant professor of microbiology, and Evgeni Sokurenko, UW professor of microbiology, and their research teams are collaborating to understand the evolutionary consequences of these conflicts. The major focus of Merrikh and her research team is on understanding mechanistic and physiological aspects of conflicts in living cells – including why and how these collisions lead to mutations.

      Impediments to replication, they noted, can cause instability within the genome, such as chromosome deletions or rearrangements, or incomplete separation of genetic material during cell division. When dangerous collisions take place, bacteria sometimes employ methods to repair, and then restart, the paused DNA replication, Merrikh discovered in her earlier work at the Massachusetts Institute of Technology.

      To avoid unwanted encounters, bacteria orient most of their genes along what is called the leading strand of DNA, rather than the lagging. The terms refer to the direction the encoding activities travel on different forks of the unwinding DNA. Head-on collisions between replication and transcription happen on the lagging strand.

      Despite the heightened risk of gene-altering clashes, the study bacteria B. subtilis still orients 25 percent of all its genes, and 6 percent of its essential genes, on the lagging strand.

      The scientist observed that genes under the greatest natural selection pressure for amino-acid mutations, a sign of their adaptive significance, were on the lagging strand. Amino acids are the building blocks for proteins. Based on their analysis of mutations on the leading and the lagging strands, the researchers found that the rate of accumulation of mutations was faster in the genes oriented to be subject to head-on replication-transcription conflicts, in contrast to co-directional conflicts.

      According to the researchers, together the mutational analyses of the genomes and the experimental findings indicate that head-on conflicts were more likely than same-direction conflicts to cause mutations. They also found that longer genes provided more opportunities for replication-transcription conflicts to occur. Lengthy genes were more prone to mutate.

      The researchers noted that head-on replication-transcription encounters, and the subsequent mutations, could significantly increase structural variations in the proteins coded by the affected genes. Some of these chance variations might give the bacteria new options for adapting to changes or stresses in their environment. Like savvy investors, the bacteria appear to protect most of their genetic assets, but offer a few up to the high-roll stakes of mutation.

      The researchers pointed out, "A simple switch in gene orientation …could facilitate evolution in specific genes in a targeted way. Investigating the main targets of conflict-mediated formation of mutations is likely to show far-reaching insights into adaptation and evolution of organisms."

      Provided by University of Washington

      "Head-on collisions between DNA-code reading machineries accelerate gene evolution." March 29th, 2013. http://phys.org/news/2013-03-head-on-collisions-dna-code-machineries-gene.html

      Posted by
      Robert Karl Stonjek




    • Edgar Owen
      Hi James, Yes, computer simulations are a good approach to study the problem. I ve done a number of them myself... Kohl and other creationists, and I think
      Message 2 of 21 , Mar 31, 2013
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        Hi James,

        Yes, computer simulations are a good approach to study the problem. I've done a number of them myself...

        Kohl and other creationists, and I think many scientists too, don't properly analyze the problem....

        For an accurate analysis one needs to begin with the total number of base pairs in DNA, average generation intervals, mutation frequencies, and most importantly and unknown what changes to DNA produce viable offspring and which don't?

        For pure passive blueprint notion of DNA I suspect you don't get very far with just 'random mutations'. I agree that the Kohl and creationist 'random mutation' straw man IN ITSELF is not a viable explanation for all the evolved genetic diversity of life.

        Again as I suggest, what you need is an ACTIVE genetic mechanism, that itself tinkers with changes to DNA and then error corrects and tries to reshuffle to produce viable organisms... There is more and more evidence that all sorts of such mechanisms exist. It is these mechanisms working on DNA, and the inevitable errors that occur in it, that is responsible for the variations that evolution selects among, and not just passive blueprint non error correctable DNA that Kohl and the creationists envision...

        Edgar



        On Mar 31, 2013, at 12:32 AM, James Gray wrote:

        > Edgar,
        > I have to thank you for writing this. I have never seen Kohl admit or deny
        > that he was a creationist. At least this gives me an idea what the random
        > mutation theory is that Kohl will not describe but calls ridiculous.
        > However, I do not see how even a random mutation theory that worked on a
        > passive blueprint would fail as long as the replication was reasonably
        > good. About 20 years ago I wrote a simulation using a dedicated computer
        > using the language M. It is relatively easy to write M code that can write
        > M code. It easy for a job running in M to spin off another job. The only
        > problem is that the replication is essentially perfect. To simulate random
        > mutation I had to have a separate reproduction module that the replicators
        > would call to replicate themselves. As long as the fidelity was fairly
        > high, random mutation worked. I did have the reproduction module make
        > totally random errors meaning arbitrary substitution of ASCII characters.
        > It also randomly duplicated lines of code and randomly deleted lines of
        > code. There was one arbitrary non-random mutation I allowed to occur
        > randomly. The ability to kill competitor jobs. To make the simulation
        > life like I had to arbitrarily limit the life expectancy of each job. The
        > only resources the jobs competed for was CPU cycles and partition space.
        > One problem was that because of looping in software is that it was way to
        > easy for the jobs to discover the secret to eternal life. I did have
        > instances where things ran for a while and then everything went extinct.
        >
        > James Gray
        >
        > On Sat, Mar 30, 2013 at 7:29 AM, Edgar Owen <edgarowen@...> wrote:
        >
        >> **
        >>
        >>
        >> All,
        >>
        >> As evidenced in the post below and many many others clearly most genetic
        >> changes occur via internal replicative mechanisms and NOT Kohl's "random
        >> mutation" straw man.
        >>
        >> But neither do they occur via what these bacteria ate or smelled as Kohl's
        >> nutty 'model' would have us believe... What an organism eats or smells does
        >> produce some minimal epigenetic changes but they DO NOT alter the genetic
        >> code.
        >>
        >> There are natural internal replicative mechanisms that are responsible for
        >> nearly all genetic changes. Meiosis is the most obvious, but there are many
        >> others, such as copying errors, that produce more profound changes.
        >>
        >> The key to understanding this is to recognize the power of DNA to produce
        >> viable organisms. Even in the face of radical changes the micro genetic
        >> machinery is highly self correcting towards producing viable organisms even
        >> in the face of considerable 'damage' some of which can be produced by
        >> random mutations. Go in and mess the DNA up and the internal mechanisms
        >> always try to patch it up so that it produces a viable organism even if
        >> that viable organism is a new organism with new genetics.
        >>
        >> The internal genetic machinery is not a simple passive blueprint, it is an
        >> active system that above all tries to produce a viable organism from a
        >> large repertoire of elemental building blocks, no matter if or how those
        >> building blocks have been reshuffled or even damaged.
        >>
        >>
        >> The 'random mutation' theory is a standard CREATIONIST (yes Kohl is a self
        >> admitted creationist) straw man that assumes DNA is a passive blueprint,
        >> rather than part of the active system I describe above.
        >>
        >> Random mutations, to the extent they are responsible for genetic change,
        >> tend to work to elicit reshufflings of the basic building blocks by active
        >> internal mechanisms, rather than simply changing something in a passive
        >> fixed blueprint every bit of which must remain exact to produce a viable
        >> organism.
        >>
        >> Edgar
        >>
        >>
        >>
        >> On Mar 29, 2013, at 9:29 PM, Robert Karl Stonjek wrote:
        >>
        >>
        >>
        >> <http://phys.org/>
        >> Head-on collisions between DNA-code reading machineries accelerate gene
        >> evolutionMarch 29th, 2013 in Biology / Cell & Microbiology
        >> [image: Head-on collisions between DNA-code reading machineries accelerate
        >> gene evolution]Enlarge<http://cdn.physorg.com/newman/gfx/news/hires/2013/headoncollis.jpg>
        >>
        >> *Houra Merrikh, assistant professor of microbiology, and her student
        >> Samuel Million-Weaver, University of Washington, study mechanisms that
        >> bacteria use to evolve and adapt. Credit: Christopher Merrikh*
        >>
        >> *Bacteria appear to speed up their evolution by positioning specific
        >> genes along the route of expected traffic jams in DNA encoding. Certain
        >> genes are in prime collision paths for the moving molecular machineries
        >> that read the DNA code, as University of Washington scientists explain in
        >> this week's edition of Nature.*
        >>
        >> The spatial-organization tactics their model organism, *Bacillus subtilis*,
        >> takes to evolve and adapt might be imitated in other related Gram-positive
        >> bacteria, including harmful, ever-changing germs like staph, strep, and
        >> listeria, to strengthen their virulence or cause persistent infections. The
        >> researchers think that these mechanisms for accelerating evolution may be
        >> found in other living creatures as well.
        >>
        >> Replication – the duplicating of the genetic code to create a new set of
        >> genes– and transcription – the copying of DNA code to produce a protein –
        >> are not separated by time or space in bacteria. Therefore, clashes between
        >> these machineries are inevitable. Replication traveling rapidly along a DNA
        >> strand can be stalled by a head-on encounter or same-direction brush with
        >> slower-moving transcription.
        >>
        >> The senior authors of the study, Houra Merrikh, UW assistant professor of
        >> microbiology, and Evgeni Sokurenko, UW professor of microbiology, and their
        >> research teams are collaborating to understand the evolutionary
        >> consequences of these conflicts. The major focus of Merrikh and her
        >> research team is on understanding mechanistic and physiological aspects of
        >> conflicts in living cells – including why and how these collisions lead to
        >> mutations.
        >>
        >> Impediments to replication, they noted, can cause instability within the
        >> genome, such as chromosome deletions or rearrangements, or incomplete
        >> separation of genetic material during cell division. When dangerous
        >> collisions take place, bacteria sometimes employ methods to repair, and
        >> then restart, the paused DNA replication, Merrikh discovered in her earlier
        >> work at the Massachusetts Institute of Technology.
        >>
        >> To avoid unwanted encounters, bacteria orient most of their genes along
        >> what is called the leading strand of DNA, rather than the lagging. The
        >> terms refer to the direction the encoding activities travel on different
        >> forks of the unwinding DNA. Head-on collisions between replication and
        >> transcription happen on the lagging strand.
        >>
        >> Despite the heightened risk of gene-altering clashes, the study bacteria *B.
        >> subtilis* still orients 25 percent of all its genes, and 6 percent of its
        >> essential genes, on the lagging strand.
        >>
        >> The scientist observed that genes under the greatest natural selection
        >> pressure for amino-acid mutations, a sign of their adaptive significance,
        >> were on the lagging strand. Amino acids are the building blocks for
        >> proteins. Based on their analysis of mutations on the leading and the
        >> lagging strands, the researchers found that the rate of accumulation of
        >> mutations was faster in the genes oriented to be subject to head-on
        >> replication-transcription conflicts, in contrast to co-directional
        >> conflicts.
        >>
        >> According to the researchers, together the mutational analyses of the
        >> genomes and the experimental findings indicate that head-on conflicts were
        >> more likely than same-direction conflicts to cause mutations. They also
        >> found that longer genes provided more opportunities for
        >> replication-transcription conflicts to occur. Lengthy genes were more prone
        >> to mutate.
        >>
        >> The researchers noted that head-on replication-transcription encounters,
        >> and the subsequent mutations, could significantly increase structural
        >> variations in the proteins coded by the affected genes. Some of these
        >> chance variations might give the bacteria new options for adapting to
        >> changes or stresses in their environment. Like savvy investors, the
        >> bacteria appear to protect most of their genetic assets, but offer a few up
        >> to the high-roll stakes of mutation.
        >>
        >> The researchers pointed out, "A simple switch in gene orientation …could
        >> facilitate evolution in specific genes in a targeted way. Investigating the
        >> main targets of conflict-mediated formation of mutations is likely to show
        >> far-reaching insights into adaptation and evolution of organisms."
        >>
        >> Provided by University of Washington
        >>
        >> **
        >>
        >> "Head-on collisions between DNA-code reading machineries accelerate gene
        >> evolution." March 29th, 2013.
        >> http://phys.org/news/2013-03-head-on-collisions-dna-code-machineries-gene.html
        >>
        >> Posted by
        >> Robert Karl Stonjek
        >>
        >>
        >>
        >>
      • Nils K.
        Dear James, dear All! James Grey: ... I did have instances where things ran for a while and then everything went extinct .... NKO: Did you have instances where
        Message 3 of 21 , Mar 31, 2013
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          Dear James, dear All!

          James Grey:
          ... I did have instances where things ran for a while and
          then everything went extinct ....

          NKO:
          Did you have instances where things did not go extinct?

          We do know (or at least we do think we know) that mutations are
          random. However, we have enormous, probably unsolvable, problems
          with the very meaning of "random". GRT is deterministic, and QT (QM)
          does have, as a whole, an undisputed deterministic interpretation
          (David Bohm) who successfully pushed the randomness of QM back to
          the very beginning of Big Bang. Large parts of QM were already
          deterministic before Bohm's interpretation, for example the
          Schroedinger's equation. Einstein did not believe in genuine
          randomness. The Aspect experiments and similar experiments, after
          Einstein's death, did show that we do have non-local determinism
          as well, but these experiments did not rule out local causation
          or local determinism. They are somewhat unclear statistical
          experiments, not totally ruling out Einstein's claims. Experts
          say that if Einstein was alive today, he would not change his mind
          about these problems.

          So, we are back to Kant: We cannot understand Das Ding An Sich.

          Randomness bellongs to Das Ding An Sich. We now do have one foot
          in the philosophy of religion, just as the cosmologists do have.
          Already the Singularity that created BB "something" knew that
          biological evolution on planets was to happen. This Singularity
          represented unlimited complexity (measured as order), and is a
          perfect creator candidate. However, the Big Bang IS a CREATION,
          in all imaginable ways. Biological evolution, in itself, is
          only a small part of the CREATION.

          Dawkins' equation: Evolution exists equals a creator/creation
          does not exist, is logically wrong. Moreover, this equation is
          contradicting all cosmological evidences.

          Apropos random mutations. Next to all mutations are gene damage --
          just because they are random. Mathematics can tell us that it is
          impossible to remove this flow of damaged DNA from the populations
          by means of the many known mechanisms to remove bad DNA.
          Moreover, close inspections of individual deaths of organisms,
          show that nearly all deaths are random and have nothing to do with
          the individuals having bad DNA.

          Finally, we have the several DNA repair mechanisms which work
          against genetic change. And we have the many living fossils, the
          Cambrian explosion, and other mysteries of evolutuion which are
          impossible to explain. As if these things are not enough: Junk DNA
          is now discovered to not being junk DNA.

          Best,
          NKO
        • james kohl
          James Gray: I would like to see an explanation in lay person terms of what his alternative to random mutations is and why anyone would think that random
          Message 4 of 21 , Mar 31, 2013
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            James Gray: I would like to see an explanation in lay person terms of what his alternative to random mutations is and why anyone would think that random mutations is a ridiculous idea.

             

            My reply:

            JK: What an organism eats determines its pheromone production, which controls the species reproduction…. An opposing model organism for random mutations theory is the peppered moth species. Industrial pollution supposedly caused random mutations and the color change from light to dark.  Natural selection based on the color change then caused the darker color to prevail until pollution was controlled, which is when the change back to the lighter color occurred (via random mutations). 

            Maybe someone can explain in layperson's terms what that means in the context of evolution of the peppered moth species, or any other species. If random mutations cause the color change, my model is not necessary. However, it will still be necessary for someone to tell us how the theory of the color change might be included in a broader based theory of adaptive evolution.

            James Gray: Edgar, I have to thank you for writing this.

             

            I have to thank James Gray for thanking Edgar for bastardizing my reply to the group, and specifically my reply to the request James Gray made. After I explained my model, which is an alternative to random mutations theory, in layperson's terms, Gray thanks Edgar with no response to me whatsoever, despite my use of model organisms in my explanation. Thanking Edgar, who is arguably even more ignorant than James Gray is in the context of this discussion, and then continuing to ignore any aspect of my model, exemplifies the fact that James Gray will continue to choose ignorance instead of common sense.

             

            COMMON SENSE: What an organism eats determines its pheromone production, which controls the species reproduction. James Gray won’t read anything that supplies the details of how: "Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans." And no one is telling us how random mutations or anything else enables natural selection and adaptive evolution. For contrast, as with the peppered moth, here is an excerpt from a report on a study of butterflies: We have shown that the olfactory signal of inbred males was the sole trait causally responsible for their decreased mating success.     

             

            The fools have won out over common sense and details of biological facts (i.e., nutrient-dependent pheromone-controlled adaptive evolution). Like James Gray, you should thank the fools for that – if you also wish to remain ignorant and look towards Edgar for information on pheromones – or anything else.

             
            James V. Kohl
            Medical laboratory scientist (ASCP)
            Independent researcher
            Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.



            From: Edgar Owen <edgarowen@...>
            To: evolutionary-psychology@yahoogroups.com
            Sent: Sun, March 31, 2013 10:15:24 AM
            Subject: Re: [evol-psych] The truth about RANDOM MUTATIONS.

            Hi James,

            Yes, computer simulations are a good approach to study the problem. I've done a number of them myself...

            Kohl and other creationists, and I think many scientists too, don't properly analyze the problem....

            For an accurate analysis one needs to begin with the total number of base pairs in DNA, average generation intervals, mutation frequencies, and most importantly and unknown what changes to DNA produce viable offspring and which don't?

            For pure passive blueprint notion of DNA I suspect you don't get very far with just 'random mutations'. I agree that the Kohl and creationist 'random mutation' straw man IN ITSELF is not a viable explanation for all the evolved genetic diversity of life.

            Again as I suggest, what you need is an ACTIVE genetic mechanism, that itself tinkers with changes to DNA and then error corrects and tries to reshuffle to produce viable organisms... There is more and more evidence that all sorts of such mechanisms exist. It is these mechanisms working on DNA, and the inevitable errors that occur in it, that is responsible for the variations that evolution selects among, and not just passive blueprint non error correctable DNA that Kohl and the creationists envision...

            Edgar



            On Mar 31, 2013, at 12:32 AM, James Gray wrote:

            > Edgar,
            > I have to thank you for writing this.  I have never seen Kohl admit or deny
            > that he was a creationist.  At least this gives me an idea what the random
            > mutation theory is that Kohl will not describe but calls ridiculous.
            > However, I do not see how even a random mutation theory that worked on a
            > passive blueprint would fail as long as the replication was reasonably
            > good.  About 20 years ago I wrote a simulation using a dedicated computer
            > using the language M.  It is relatively easy to write M code that can write
            > M code.  It easy for a job running in M to spin off another job.  The only
            > problem is that the replication is essentially perfect.  To simulate random
            > mutation I had to have a separate reproduction module that the replicators
            > would call to replicate themselves.  As long as the fidelity was fairly
            > high, random mutation worked.  I did have the reproduction module make
            > totally random errors meaning arbitrary substitution of ASCII characters.
            > It also randomly duplicated lines of code and randomly deleted lines of
            > code.  There was one arbitrary non-random mutation I allowed to occur
            > randomly.  The ability to kill competitor jobs.  To make the simulation
            > life like I had to arbitrarily limit the life expectancy of each job.  The
            > only resources the jobs competed for was CPU cycles and partition space.
            > One problem was that because of looping in software is that it was way to
            > easy for the jobs to discover the secret to eternal life.  I did have
            > instances where things ran for a while and then everything went extinct.
            >
            > James Gray
            >
            > On Sat, Mar 30, 2013 at 7:29 AM, Edgar Owen <edgarowen@...> wrote:
            >
            >> **
            >>
            >>
            >> All,
            >>
            >> As evidenced in the post below and many many others clearly most genetic
            >> changes occur via internal replicative mechanisms and NOT Kohl's "random
            >> mutation" straw man.
            >>
            >> But neither do they occur via what these bacteria ate or smelled as Kohl's
            >> nutty 'model' would have us believe... What an organism eats or smells does
            >> produce some minimal epigenetic changes but they DO NOT alter the genetic
            >> code.
            >>
            >> There are natural internal replicative mechanisms that are responsible for
            >> nearly all genetic changes. Meiosis is the most obvious, but there are many
            >> others, such as copying errors, that produce more profound changes.
            >>
            >> The key to understanding this is to recognize the power of DNA to produce
            >> viable organisms. Even in the face of radical changes the micro genetic
            >> machinery is highly self correcting towards producing viable organisms even
            >> in the face of considerable 'damage' some of which can be produced by
            >> random mutations. Go in and mess the DNA up and the internal mechanisms
            >> always try to patch it up so that it produces a viable organism even if
            >> that viable organism is a new organism with new genetics.
            >>
            >> The internal genetic machinery is not a simple passive blueprint, it is an
            >> active system that above all tries to produce a viable organism from a
            >> large repertoire of elemental building blocks, no matter if or how those
            >> building blocks have been reshuffled or even damaged.
            >>
            >>
            >> The 'random mutation' theory is a standard CREATIONIST (yes Kohl is a self
            >> admitted creationist) straw man that assumes DNA is a passive blueprint,
            >> rather than part of the active system I describe above.
            >>
            >> Random mutations, to the extent they are responsible for genetic change,
            >> tend to work to elicit reshufflings of the basic building blocks by active
            >> internal mechanisms, rather than simply changing something in a passive
            >> fixed blueprint every bit of which must remain exact to produce a viable
            >> organism.
            >>
            >> Edgar
            >>
            >>
            >>
            >> On Mar 29, 2013, at 9:29 PM, Robert Karl Stonjek wrote:
            >>
            >>
            >>
            >> <http://phys.org/>
            >> Head-on collisions between DNA-code reading machineries accelerate gene
            >> evolutionMarch 29th, 2013 in Biology / Cell & Microbiology
            >> [image: Head-on collisions between DNA-code reading machineries accelerate
            >> gene evolution]Enlarge<http://cdn.physorg.com/newman/gfx/news/hires/2013/headoncollis.jpg>
            >>
            >> *Houra Merrikh, assistant professor of microbiology, and her student
            >> Samuel Million-Weaver, University of Washington, study mechanisms that
            >> bacteria use to evolve and adapt. Credit: Christopher Merrikh*
            >>
            >> *Bacteria appear to speed up their evolution by positioning specific
            >> genes along the route of expected traffic jams in DNA encoding. Certain
            >> genes are in prime collision paths for the moving molecular machineries
            >> that read the DNA code, as University of Washington scientists explain in
            >> this week's edition of Nature.*
            >>
            >> The spatial-organization tactics their model organism, *Bacillus subtilis*,
            >> takes to evolve and adapt might be imitated in other related Gram-positive
            >> bacteria, including harmful, ever-changing germs like staph, strep, and
            >> listeria, to strengthen their virulence or cause persistent infections. The
            >> researchers think that these mechanisms for accelerating evolution may be
            >> found in other living creatures as well.
            >>
            >> Replication – the duplicating of the genetic code to create a new set of
            >> genes– and transcription – the copying of DNA code to produce a protein –
            >> are not separated by time or space in bacteria. Therefore, clashes between
            >> these machineries are inevitable. Replication traveling rapidly along a DNA
            >> strand can be stalled by a head-on encounter or same-direction brush with
            >> slower-moving transcription.
            >>
            >> The senior authors of the study, Houra Merrikh, UW assistant professor of
            >> microbiology, and Evgeni Sokurenko, UW professor of microbiology, and their
            >> research teams are collaborating to understand the evolutionary
            >> consequences of these conflicts. The major focus of Merrikh and her
            >> research team is on understanding mechanistic and physiological aspects of
            >> conflicts in living cells – including why and how these collisions lead to
            >> mutations.
            >>
            >> Impediments to replication, they noted, can cause instability within the
            >> genome, such as chromosome deletions or rearrangements, or incomplete
            >> separation of genetic material during cell division. When dangerous
            >> collisions take place, bacteria sometimes employ methods to repair, and
            >> then restart, the paused DNA replication, Merrikh discovered in her earlier
            >> work at the Massachusetts Institute of Technology.
            >>
            >> To avoid unwanted encounters, bacteria orient most of their genes along
            >> what is called the leading strand of DNA, rather than the lagging. The
            >> terms refer to the direction the encoding activities travel on different
            >> forks of the unwinding DNA. Head-on collisions between replication and
            >> transcription happen on the lagging strand.
            >>
            >> Despite the heightened risk of gene-altering clashes, the study bacteria *B.
            >> subtilis* still orients 25 percent of all its genes, and 6 percent of its
            >> essential genes, on the lagging strand.
            >>
            >> The scientist observed that genes under the greatest natural selection
            >> pressure for amino-acid mutations, a sign of their adaptive significance,
            >> were on the lagging strand. Amino acids are the building blocks for
            >> proteins. Based on their analysis of mutations on the leading and the
            >> lagging strands, the researchers found that the rate of accumulation of
            >> mutations was faster in the genes oriented to be subject to head-on
            >> replication-transcription conflicts, in contrast to co-directional
            >> conflicts.
            >>
            >> According to the researchers, together the mutational analyses of the
            >> genomes and the experimental findings indicate that head-on conflicts were
            >> more likely than same-direction conflicts to cause mutations. They also
            >> found that longer genes provided more opportunities for
            >> replication-transcription conflicts to occur. Lengthy genes were more prone
            >> to mutate.
            >>
            >> The researchers noted that head-on replication-transcription encounters,
            >> and the subsequent mutations, could significantly increase structural
            >> variations in the proteins coded by the affected genes. Some of these
            >> chance variations might give the bacteria new options for adapting to
            >> changes or stresses in their environment. Like savvy investors, the
            >> bacteria appear to protect most of their genetic assets, but offer a few up
            >> to the high-roll stakes of mutation.
            >>
            >> The researchers pointed out, "A simple switch in gene orientation …could
            >> facilitate evolution in specific genes in a targeted way. Investigating the
            >> main targets of conflict-mediated formation of mutations is likely to show
            >> far-reaching insights into adaptation and evolution of organisms."
            >>
            >> Provided by University of Washington
            >>
            >> **
            >>
            >> "Head-on collisions between DNA-code reading machineries accelerate gene
            >> evolution." March 29th, 2013.
            >> http://phys.org/news/2013-03-head-on-collisions-dna-code-machineries-gene.html
            >>
            >> Posted by
            >> Robert Karl Stonjek
            >>
            >>
            >>
            >>



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          • Leif Ekblad
            Hi Edgar, I agree. In fact, I m pretty sure that today s knowledge of the genome is not suffcient to explain species typical differences. The person that
            Message 5 of 21 , Mar 31, 2013
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              Hi Edgar,

              I agree.

              In fact, I'm pretty sure that today's knowledge of the genome is not
              suffcient to explain species typical differences. The person that figures
              out how this works might get the next nobel price. But just because we don't
              know how this works at the DNA level, it doesn't mean we should accept that
              it is epigenetic. Today epigenetic seems to be a popular way to claim to be
              able to understand complex issues that we cannot explain with genes alone.
              There should be just as much requirements for real proof on epigenetics as
              there is for genetics.

              Leif Ekblad


              ----- Original Message -----
              From: "Edgar Owen" <edgarowen@...>
              To: <evolutionary-psychology@yahoogroups.com>
              Sent: Sunday, March 31, 2013 3:00 PM
              Subject: Re: [evol-psych] The truth about RANDOM MUTATIONS.


              Hi James,

              Yes, computer simulations are a good approach to study the problem. I've
              done a number of them myself...

              Kohl and other creationists, and I think many scientists too, don't properly
              analyze the problem....

              For an accurate analysis one needs to begin with the total number of base
              pairs in DNA, average generation intervals, mutation frequencies, and most
              importantly and unknown what changes to DNA produce viable offspring and
              which don't?

              For pure passive blueprint notion of DNA I suspect you don't get very far
              with just 'random mutations'. I agree that the Kohl and creationist 'random
              mutation' straw man IN ITSELF is not a viable explanation for all the
              evolved genetic diversity of life.

              Again as I suggest, what you need is an ACTIVE genetic mechanism, that
              itself tinkers with changes to DNA and then error corrects and tries to
              reshuffle to produce viable organisms... There is more and more evidence
              that all sorts of such mechanisms exist. It is these mechanisms working on
              DNA, and the inevitable errors that occur in it, that is responsible for the
              variations that evolution selects among, and not just passive blueprint non
              error correctable DNA that Kohl and the creationists envision...

              Edgar



              On Mar 31, 2013, at 12:32 AM, James Gray wrote:

              > Edgar,
              > I have to thank you for writing this. I have never seen Kohl admit or
              > deny
              > that he was a creationist. At least this gives me an idea what the random
              > mutation theory is that Kohl will not describe but calls ridiculous.
              > However, I do not see how even a random mutation theory that worked on a
              > passive blueprint would fail as long as the replication was reasonably
              > good. About 20 years ago I wrote a simulation using a dedicated computer
              > using the language M. It is relatively easy to write M code that can
              > write
              > M code. It easy for a job running in M to spin off another job. The only
              > problem is that the replication is essentially perfect. To simulate
              > random
              > mutation I had to have a separate reproduction module that the replicators
              > would call to replicate themselves. As long as the fidelity was fairly
              > high, random mutation worked. I did have the reproduction module make
              > totally random errors meaning arbitrary substitution of ASCII characters.
              > It also randomly duplicated lines of code and randomly deleted lines of
              > code. There was one arbitrary non-random mutation I allowed to occur
              > randomly. The ability to kill competitor jobs. To make the simulation
              > life like I had to arbitrarily limit the life expectancy of each job. The
              > only resources the jobs competed for was CPU cycles and partition space.
              > One problem was that because of looping in software is that it was way to
              > easy for the jobs to discover the secret to eternal life. I did have
              > instances where things ran for a while and then everything went extinct.
              >
              > James Gray
              >
              > On Sat, Mar 30, 2013 at 7:29 AM, Edgar Owen <edgarowen@...> wrote:
              >
              <snip>
            • Leif Ekblad
              JK: What an organism eats determines its pheromone production, which controls the species reproduction…. An opposing model organism for random mutations
              Message 6 of 21 , Mar 31, 2013
              • 0 Attachment
                
                JK: What an organism eats determines its pheromone production, which controls the species reproduction…. An opposing model organism for random mutations theory is the peppered moth species. Industrial pollution supposedly caused random mutations and the color change from light to dark.  Natural selection based on the color change then caused the darker color to prevail until pollution was controlled, which is when the change back to the lighter color occurred (via random mutations). 
                 
                Leif Ekblad: According to wikipedia (http://en.wikipedia.org/wiki/Peppered_moth_evolution) what you are proposing makes no sense. First, the specific mutation responsible for the color change is known. Second, dark color is dominant, which can account for the fast switch in color. Third, it is possible that both types existed before pollution started, and was involved in balanced selection, so there really was no need for a mutation when pollution started, only selection on the darker types. Forth, there is no need for a back-mutation as all that needs to happen is new selection on the light phenotype which will increase its frequency.
                 
                In short, moth evolution doesn't support your model, doesn't support an epigenetic model, but instead have strong evidence for a mutation determining color.
                 
                Leif Ekblad
                 
              • Michael Lamport Commons
                I really do not understand this discussion. There are errors in replication that have many sources, radiation, oxidation, and other sources of errors. One can
                Message 7 of 21 , Mar 31, 2013
                • 0 Attachment
                  I really do not understand this discussion.

                  There are errors in replication that have many sources, radiation, oxidation, and other sources of errors.  One can observe these changes in the development of cancer, and in aging.  So what is this all about?  Also proving randomness is like proving the null hypotheses.  All one can observe is errors in replication
                  My Best,
                  
                  Michael Lamport Commons, Ph.D.
                  Assistant Clinical Professor
                  
                  Department of Psychiatry
                  Beth Israel Deaconess Medical Center
                  Harvard Medical School
                  234 Huron Avenue
                  Cambridge, MA 02138-1328
                  
                  Telephone  (617) 497-5270
                  Facsimile   (617) 491-5270
                  Cellular      (617) 320 0896
                  Commons@...
                  http://dareassociation.org/
                  Skype: MichaelCommons
                  
                  
                  
                  On 3/31/2013 9:00 AM, Edgar Owen wrote:
                  Hi James,
                  
                  Yes, computer simulations are a good approach to study the problem. I've done a number of them myself...
                  
                  Kohl and other creationists, and I think many scientists too, don't properly analyze the problem.... 
                  
                  For an accurate analysis one needs to begin with the total number of base pairs in DNA, average generation intervals, mutation frequencies, and most importantly and unknown what changes to DNA produce viable offspring and which don't?
                  
                  For pure passive blueprint notion of DNA I suspect you don't get very far with just 'random mutations'. I agree that the Kohl and creationist 'random mutation' straw man IN ITSELF is not a viable explanation for all the evolved genetic diversity of life.
                  
                  Again as I suggest, what you need is an ACTIVE genetic mechanism, that itself tinkers with changes to DNA and then error corrects and tries to reshuffle to produce viable organisms... There is more and more evidence that all sorts of such mechanisms exist. It is these mechanisms working on DNA, and the inevitable errors that occur in it, that is responsible for the variations that evolution selects among, and not just passive blueprint non error correctable DNA that Kohl and the creationists envision...
                  
                  Edgar
                  
                  
                  
                  On Mar 31, 2013, at 12:32 AM, James Gray wrote:
                  
                  
                  Edgar,
                  I have to thank you for writing this.  I have never seen Kohl admit or deny
                  that he was a creationist.  At least this gives me an idea what the random
                  mutation theory is that Kohl will not describe but calls ridiculous.
                  However, I do not see how even a random mutation theory that worked on a
                  passive blueprint would fail as long as the replication was reasonably
                  good.  About 20 years ago I wrote a simulation using a dedicated computer
                  using the language M.  It is relatively easy to write M code that can write
                  M code.  It easy for a job running in M to spin off another job.  The only
                  problem is that the replication is essentially perfect.  To simulate random
                  mutation I had to have a separate reproduction module that the replicators
                  would call to replicate themselves.  As long as the fidelity was fairly
                  high, random mutation worked.  I did have the reproduction module make
                  totally random errors meaning arbitrary substitution of ASCII characters.
                  It also randomly duplicated lines of code and randomly deleted lines of
                  code.  There was one arbitrary non-random mutation I allowed to occur
                  randomly.  The ability to kill competitor jobs.  To make the simulation
                  life like I had to arbitrarily limit the life expectancy of each job.  The
                  only resources the jobs competed for was CPU cycles and partition space.
                  One problem was that because of looping in software is that it was way to
                  easy for the jobs to discover the secret to eternal life.  I did have
                  instances where things ran for a while and then everything went extinct.
                  
                  James Gray
                  
                  On Sat, Mar 30, 2013 at 7:29 AM, Edgar Owen <edgarowen@...> wrote:
                  
                  
                  **
                  
                  
                  All,
                  
                  As evidenced in the post below and many many others clearly most genetic
                  changes occur via internal replicative mechanisms and NOT Kohl's "random
                  mutation" straw man.
                  
                  But neither do they occur via what these bacteria ate or smelled as Kohl's
                  nutty 'model' would have us believe... What an organism eats or smells does
                  produce some minimal epigenetic changes but they DO NOT alter the genetic
                  code.
                  
                  There are natural internal replicative mechanisms that are responsible for
                  nearly all genetic changes. Meiosis is the most obvious, but there are many
                  others, such as copying errors, that produce more profound changes.
                  
                  The key to understanding this is to recognize the power of DNA to produce
                  viable organisms. Even in the face of radical changes the micro genetic
                  machinery is highly self correcting towards producing viable organisms even
                  in the face of considerable 'damage' some of which can be produced by
                  random mutations. Go in and mess the DNA up and the internal mechanisms
                  always try to patch it up so that it produces a viable organism even if
                  that viable organism is a new organism with new genetics.
                  
                  The internal genetic machinery is not a simple passive blueprint, it is an
                  active system that above all tries to produce a viable organism from a
                  large repertoire of elemental building blocks, no matter if or how those
                  building blocks have been reshuffled or even damaged.
                  
                  
                  The 'random mutation' theory is a standard CREATIONIST (yes Kohl is a self
                  admitted creationist) straw man that assumes DNA is a passive blueprint,
                  rather than part of the active system I describe above.
                  
                  Random mutations, to the extent they are responsible for genetic change,
                  tend to work to elicit reshufflings of the basic building blocks by active
                  internal mechanisms, rather than simply changing something in a passive
                  fixed blueprint every bit of which must remain exact to produce a viable
                  organism.
                  
                  Edgar
                  
                  
                  
                  On Mar 29, 2013, at 9:29 PM, Robert Karl Stonjek wrote:
                  
                  
                  
                  <http://phys.org/>
                  Head-on collisions between DNA-code reading machineries accelerate gene
                  evolutionMarch 29th, 2013 in Biology / Cell & Microbiology
                  [image: Head-on collisions between DNA-code reading machineries accelerate
                  gene evolution]Enlarge<http://cdn.physorg.com/newman/gfx/news/hires/2013/headoncollis.jpg>
                  
                  *Houra Merrikh, assistant professor of microbiology, and her student
                  Samuel Million-Weaver, University of Washington, study mechanisms that
                  bacteria use to evolve and adapt. Credit: Christopher Merrikh*
                  
                  *Bacteria appear to speed up their evolution by positioning specific
                  genes along the route of expected traffic jams in DNA encoding. Certain
                  genes are in prime collision paths for the moving molecular machineries
                  that read the DNA code, as University of Washington scientists explain in
                  this week's edition of Nature.*
                  
                  The spatial-organization tactics their model organism, *Bacillus subtilis*,
                  takes to evolve and adapt might be imitated in other related Gram-positive
                  bacteria, including harmful, ever-changing germs like staph, strep, and
                  listeria, to strengthen their virulence or cause persistent infections. The
                  researchers think that these mechanisms for accelerating evolution may be
                  found in other living creatures as well.
                  
                  Replication – the duplicating of the genetic code to create a new set of
                  genes– and transcription – the copying of DNA code to produce a protein –
                  are not separated by time or space in bacteria. Therefore, clashes between
                  these machineries are inevitable. Replication traveling rapidly along a DNA
                  strand can be stalled by a head-on encounter or same-direction brush with
                  slower-moving transcription.
                  
                  The senior authors of the study, Houra Merrikh, UW assistant professor of
                  microbiology, and Evgeni Sokurenko, UW professor of microbiology, and their
                  research teams are collaborating to understand the evolutionary
                  consequences of these conflicts. The major focus of Merrikh and her
                  research team is on understanding mechanistic and physiological aspects of
                  conflicts in living cells – including why and how these collisions lead to
                  mutations.
                  
                  Impediments to replication, they noted, can cause instability within the
                  genome, such as chromosome deletions or rearrangements, or incomplete
                  separation of genetic material during cell division. When dangerous
                  collisions take place, bacteria sometimes employ methods to repair, and
                  then restart, the paused DNA replication, Merrikh discovered in her earlier
                  work at the Massachusetts Institute of Technology.
                  
                  To avoid unwanted encounters, bacteria orient most of their genes along
                  what is called the leading strand of DNA, rather than the lagging. The
                  terms refer to the direction the encoding activities travel on different
                  forks of the unwinding DNA. Head-on collisions between replication and
                  transcription happen on the lagging strand.
                  
                  Despite the heightened risk of gene-altering clashes, the study bacteria *B.
                  subtilis* still orients 25 percent of all its genes, and 6 percent of its
                  essential genes, on the lagging strand.
                  
                  The scientist observed that genes under the greatest natural selection
                  pressure for amino-acid mutations, a sign of their adaptive significance,
                  were on the lagging strand. Amino acids are the building blocks for
                  proteins. Based on their analysis of mutations on the leading and the
                  lagging strands, the researchers found that the rate of accumulation of
                  mutations was faster in the genes oriented to be subject to head-on
                  replication-transcription conflicts, in contrast to co-directional
                  conflicts.
                  
                  According to the researchers, together the mutational analyses of the
                  genomes and the experimental findings indicate that head-on conflicts were
                  more likely than same-direction conflicts to cause mutations. They also
                  found that longer genes provided more opportunities for
                  replication-transcription conflicts to occur. Lengthy genes were more prone
                  to mutate.
                  
                  The researchers noted that head-on replication-transcription encounters,
                  and the subsequent mutations, could significantly increase structural
                  variations in the proteins coded by the affected genes. Some of these
                  chance variations might give the bacteria new options for adapting to
                  changes or stresses in their environment. Like savvy investors, the
                  bacteria appear to protect most of their genetic assets, but offer a few up
                  to the high-roll stakes of mutation.
                  
                  The researchers pointed out, "A simple switch in gene orientation …could
                  facilitate evolution in specific genes in a targeted way. Investigating the
                  main targets of conflict-mediated formation of mutations is likely to show
                  far-reaching insights into adaptation and evolution of organisms."
                  
                  Provided by University of Washington
                  
                  **
                  
                  "Head-on collisions between DNA-code reading machineries accelerate gene
                  evolution." March 29th, 2013.
                  http://phys.org/news/2013-03-head-on-collisions-dna-code-machineries-gene.html
                  
                  Posted by
                  Robert Karl Stonjek
                  
                  
                  
                  
                  
                  
                  
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                • james kohl
                  From: Michael Lamport Commons I really do not understand this discussion. JK: It s a corruption of the topic thread: Adaptive
                  Message 8 of 21 , Mar 31, 2013
                  • 0 Attachment
                    From: Michael Lamport Commons <commons@...>



                    I really do not understand this discussion.

                    JK: It's a corruption of the topic thread: "Adaptive evolution: Mutations don't
                    win out"

                    There are errors in replication that have many sources, radiation,
                    oxidation, and other sources of errors. One can observe these changes
                    in the development of cancer, and in aging. So what is this all about?
                    Also proving randomness is like proving the null hypotheses. All one
                    can observe is errors in replication

                    JK: Most people know that errors in replication due not lead to natural
                    selection for mutations like those linked to physical and mental disorders. Most
                    people are able to understand the concept of nutrient-dependent
                    pheromone-controlled adaptive evolution, which is non-random (e.g., it
                    exemplifies the transition from pleiotropy to epistasis).


                    Some people, however, like Edgar Owen and James Gray, have so little knowledge
                    of biological facts that they think they need only regurgitate failed
                    statistical analyses and mathematical models. They continue to attempt to
                    convince others that natural selection for phenotypic characteristics is either
                    a numbers game or automagical.


                    Their approach is consistent withthe current bastardized version of Darwinian
                    theory, which does not address his nutrient-dependent pheromone-controlled
                    "Conditions of Existence"in species from microbes to man. Edgar can't even grasp
                    the difference between what was thought to be a "DNA world" but is now known to
                    be an "RNA world." The epigenetic effects of nutrients, for example, alterthe
                    microRNA / messenger RNA balance. That's how they enable the molecular
                    mechanisms of adaptive evolution, which are controlled by the metabolism of
                    nutrients to species-specific pheromones. Thus, the truth about random mutations
                    is that random mutationstheory hasno relevance to evolutionary psychology -- as
                    you can see in what these clowns have stated below.



                    James V. Kohl
                    Medical laboratory scientist (ASCP)
                    Independent researcher
                    Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the
                    socioaffective nature of evolved behaviors. Socioaffective Neuroscience &
                    Psychology, 2: 17338.


                    On 3/31/2013 9:00 AM, Edgar Owen wrote:

                    Hi James, Yes, computer simulations are a good approach to study the problem.
                    I've done a number of them myself... Kohl and other creationists, and I think
                    many scientists too, don't properly analyze the problem.... For an accurate
                    analysis one needs to begin with the total number of base pairs in DNA, average
                    generation intervals, mutation frequencies, and most importantly and unknown
                    what changes to DNA produce viable offspring and which don't? For pure passive
                    blueprint notion of DNA I suspect you don't get very far with just 'random
                    mutations'. I agree that the Kohl and creationist 'random mutation' straw man IN
                    ITSELF is not a viable explanation for all the evolved genetic diversity of
                    life. Again as I suggest, what you need is an ACTIVE genetic mechanism, that
                    itself tinkers with changes to DNA and then error corrects and tries to
                    reshuffle to produce viable organisms... There is more and more evidence that
                    all sorts of such mechanisms exist. It is these mechanisms working on DNA, and
                    the inevitable errors that occur in it, that is responsible for the variations
                    that evolution selects among, and not just passive blueprint non error
                    correctable DNA that Kohl and the creationists envision... Edgar On Mar 31,
                    2013, at 12:32 AM, James Gray wrote:

                    <snip>
                  • james kohl
                    From: Leif Ekblad  JK: What an organism eats determines its pheromone production, which controls the species reproduction…. An opposing
                    Message 9 of 21 , Mar 31, 2013
                    • 0 Attachment
                      From: Leif Ekblad <leif@...>
                      
                      JK: What an organism eats determines its pheromone production, which controls the species reproduction…. An opposing model organism for random mutations theory is the peppered moth species. Industrial pollution supposedly caused random mutations and the color change from light to dark.  Natural selection based on the color change then caused the darker color to prevail until pollution was controlled, which is when the change back to the lighter color occurred (via random mutations). 
                       
                      Leif Ekblad: According to wikipedia (http://en.wikipedia.org/wiki/Peppered_moth_evolution) what you are proposing makes no sense.

                      JK: According to the latest research The peppered moth and industrial melanism: evolution of a natural selection case study, your reliance on wikipedia makes no sense.

                       First, the specific mutation responsible for the color change is known. Second, dark color is dominant, which can account for the fast switch in color. Third, it is possible that both types existed before pollution started, and was involved in balanced selection, so there really was no need for a mutation when pollution started, only selection on the darker types. Forth, there is no need for a back-mutation as all that needs to happen is new selection on the light phenotype which will increase its frequency.
                       
                      In short, moth evolution doesn't support your model, doesn't support an epigenetic model, but instead have strong evidence for a mutation determining color.
                       
                      JK: Feeding the moth larvae a diet of leaves containing increased amount of lead and manganese caused the nutrient-dependent color change. Epistasis was achieved via the nutrient-dependent pheromone production of the female moth, which causes the observed patterns of migration (2km per night). The male moths selected for pheromones that signal nutrient-dependent reproductive fitness.  I've already mentioned this, and you continue to ignore biological facts. You want predators (birds eating the moths) to cause what is statistically represented as natural selection.

                      James V. Kohl
                      Medical laboratory scientist (ASCP)
                      Independent researcher
                      Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.




                       
                    • james kohl
                      From: Leif Ekblad In fact, I m pretty sure that today s knowledge of the genome is not suffcient to explain species typical differences. JK: We
                      Message 10 of 21 , Mar 31, 2013
                      • 0 Attachment
                        From: Leif Ekblad <leif@...>

                        In fact, I'm pretty sure that today's knowledge of the genome is not
                        suffcient to explain species typical differences.

                        JK: We explained the molecular epigenetics of species typical differences
                        in our 1996 Hormones and Behavior review article: From fertilization to adult sexual behavior

                        Gene Robinson has since extended the mammalian model to invertebrates, and
                        he will most likely receive a Nobel Prize for his works on the honeybee model organism.

                        "...behavioral epigenetics has yet to connect all its levels of analysis. It needs, and doesn’t yet have, at least one slam-dunk demonstration of all the links in a chain from behavior to neural activity to gene expression and back out again. How, for example, do biochemical events at a neuron’s nucleus affect the synaptic signaling between neurons that is the basis for all behavior?"

                        When I read this, I decided it was time to link the epigenetic effects of nutrients and pheromones to genes and to behavior, and back, so I did it and published the paper more than a year ago. The citation reads: Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338. DOI: 10.3402/snp.v2i0.17338.

                        Perhaps you've heard of it.
                         

                        James V. Kohl
                        --------------------------------------------------------------------------------------------

                        The person that figures
                        out how this works might get the next nobel price. But just because we don't
                        know how this works at the DNA level, it doesn't mean we should accept that
                        it is epigenetic. Today epigenetic seems to be a popular way to claim to be
                        able to understand complex issues that we cannot explain with genes alone.
                        There should be just as much requirements for real proof on epigenetics as
                        there is for genetics.

                        Leif Ekblad


                        ----- Original Message -----
                        From: "Edgar Owen" <edgarowen@...>
                        To: <evolutionary-psychology@yahoogroups.com>
                        Sent: Sunday, March 31, 2013 3:00 PM
                        Subject: Re: [evol-psych] The truth about RANDOM MUTATIONS.


                        Hi James,

                        Yes, computer simulations are a good approach to study the problem. I've
                        done a number of them myself...

                        Kohl and other creationists, and I think many scientists too, don't properly
                        analyze the problem....

                        For an accurate analysis one needs to begin with the total number of base
                        pairs in DNA, average generation intervals, mutation frequencies, and most
                        importantly and unknown what changes to DNA produce viable offspring and
                        which don't?

                        For pure passive blueprint notion of DNA I suspect you don't get very far
                        with just 'random mutations'. I agree that the Kohl and creationist 'random
                        mutation' straw man IN ITSELF is not a viable explanation for all the
                        evolved genetic diversity of life.

                        Again as I suggest, what you need is an ACTIVE genetic mechanism, that
                        itself tinkers with changes to DNA and then error corrects and tries to
                        reshuffle to produce viable organisms... There is more and more evidence
                        that all sorts of such mechanisms exist. It is these mechanisms working on
                        DNA, and the inevitable errors that occur in it, that is responsible for the
                        variations that evolution selects among, and not just passive blueprint non
                        error correctable DNA that Kohl and the creationists envision...

                        Edgar



                        On Mar 31, 2013, at 12:32 AM, James Gray wrote:

                        > Edgar,
                        > I have to thank you for writing this.  I have never seen Kohl admit or
                        > deny
                        > that he was a creationist.  At least this gives me an idea what the random
                        > mutation theory is that Kohl will not describe but calls ridiculous.
                        > However, I do not see how even a random mutation theory that worked on a
                        > passive blueprint would fail as long as the replication was reasonably
                        > good.  About 20 years ago I wrote a simulation using a dedicated computer
                        > using the language M.  It is relatively easy to write M code that can
                        > write
                        > M code.  It easy for a job running in M to spin off another job.  The only
                        > problem is that the replication is essentially perfect.  To simulate
                        > random
                        > mutation I had to have a separate reproduction module that the replicators
                        > would call to replicate themselves.  As long as the fidelity was fairly
                        > high, random mutation worked.  I did have the reproduction module make
                        > totally random errors meaning arbitrary substitution of ASCII characters.
                        > It also randomly duplicated lines of code and randomly deleted lines of
                        > code.  There was one arbitrary non-random mutation I allowed to occur
                        > randomly.  The ability to kill competitor jobs.  To make the simulation
                        > life like I had to arbitrarily limit the life expectancy of each job.  The
                        > only resources the jobs competed for was CPU cycles and partition space.
                        > One problem was that because of looping in software is that it was way to
                        > easy for the jobs to discover the secret to eternal life.  I did have
                        > instances where things ran for a while and then everything went extinct.
                        >
                        > James Gray
                        >
                        > On Sat, Mar 30, 2013 at 7:29 AM, Edgar Owen <edgarowen@...> wrote:
                        >
                        <snip>


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                      • Leif Ekblad
                        JK: According to the latest research The peppered moth and industrial melanism: evolution of a natural selection case study, your reliance on wikipedia makes
                        Message 11 of 21 , Apr 1, 2013
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                          JK: According to the latest research The peppered moth and industrial melanism: evolution of a natural selection case study, your reliance on wikipedia makes no sense.
                           
                          Leif Ekblad: The abstract doesn't mention your model or a link to nutrition / pheromones. The abstract mentions melanic gene frequencies, which I'd guess would be the genes / mutations mentioned on wikipedia. Therefore, at least the abstract agrees with the usual notion that it is a mutation that is causing the color change, and not nutrition / pheromones.
                           
                          JK: Feeding the moth larvae a diet of leaves containing increased amount of lead and manganese caused the nutrient-dependent color change. Epistasis was achieved via the nutrient-dependent pheromone production of the female moth, which causes the observed patterns of migration (2km per night). The male moths selected for pheromones that signal nutrient-dependent reproductive fitness.  I've already mentioned this, and you continue to ignore biological facts. You want predators (birds eating the moths) to cause what is statistically represented as natural selection.
                          Leif Ekblad:  It is possible that the color chage is related to a toxic diet rather than predation, but then I never claimed anything about what drove natural selection, only how the color is coded (through a DNA mutation, not epigenetics, nutrition or pheromones).
                           
                           
                           
                        • Edgar Owen
                          Leif, Yes, thanks for bringing some objective common sense to the discussion, not that it will do any good where Kohl is concerned... Edgar ... Leif, Yes,
                          Message 12 of 21 , Apr 1, 2013
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                            Leif,

                            Yes, thanks for bringing some objective common sense to the discussion, not that it will do any good where Kohl is concerned...

                            Edgar



                            On Mar 31, 2013, at 2:25 PM, Leif Ekblad wrote:

                             

                            

                            JK: What an organism eats determines its pheromone production, which controls the species reproduction…. An opposing model organism for random mutations theory is the peppered moth species. Industrial pollution supposedly caused random mutations and the color change from light to dark.  Natural selection based on the color change then caused the darker color to prevail until pollution was controlled, which is when the change back to the lighter color occurred (via random mutations). 
                             
                            Leif Ekblad: According to wikipedia (http://en.wikipedia.org/wiki/Peppered_moth_evolution) what you are proposing makes no sense. First, the specific mutation responsible for the color change is known. Second, dark color is dominant, which can account for the fast switch in color. Third, it is possible that both types existed before pollution started, and was involved in balanced selection, so there really was no need for a mutation when pollution started, only selection on the darker types. Forth, there is no need for a back-mutation as all that needs to happen is new selection on the light phenotype which will increase its frequency.
                             
                            In short, moth evolution doesn't support your model, doesn't support an epigenetic model, but instead have strong evidence for a mutation determining color.
                             
                            Leif Ekblad
                             


                          • Edgar Owen
                            Leif, Kohl continually cites published works as support for his model when they actually do nothing of the sort. This is one of the several ways he s
                            Message 13 of 21 , Apr 1, 2013
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                              Leif,

                              Kohl continually 'cites' published works as support for his 'model' when they actually do nothing of the sort. 

                              This is one of the several ways he's fraudulently bootstrapped his reputation out of nothing....

                              Edgar



                              On Apr 1, 2013, at 6:35 AM, Leif Ekblad wrote:

                               

                              

                              JK: According to the latest research The peppered moth and industrial melanism: evolution of a natural selection case study, your reliance on wikipedia makes no sense.
                               
                              Leif Ekblad: The abstract doesn't mention your model or a link to nutrition / pheromones. The abstract mentions melanic gene frequencies, which I'd guess would be the genes / mutations mentioned on wikipedia. Therefore, at least the abstract agrees with the usual notion that it is a mutation that is causing the color change, and not nutrition / pheromones.
                               
                              JK: Feeding the moth larvae a diet of leaves containing increased amount of lead and manganese caused the nutrient-dependent color change. Epistasis was achieved via the nutrient-dependent pheromone production of the female moth, which causes the observed patterns of migration (2km per night). The male moths selected for pheromones that signal nutrient-dependent reproductive fitness.  I've already mentioned this, and you continue to ignore biological facts. You want predators (birds eating the moths) to cause what is statistically represented as natural selection.
                              Leif Ekblad:  It is possible that the color chage is related to a toxic diet rather than predation, but then I never claimed anything about what drove natural selection, only how the color is coded (through a DNA mutation, not epigenetics, nutrition or pheromones).
                               
                               
                               


                            • james kohl
                              From: Leif Ekblad JK: According to the latest research The peppered moth and industrial melanism: evolution of a natural selection case study,
                              Message 14 of 21 , Apr 1, 2013
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                                From: Leif Ekblad <leif@...>
                                JK: According to the latest research The peppered moth and industrial melanism: evolution of a natural selection case study, your reliance on wikipedia makes no sense.
                                 
                                Leif Ekblad: The abstract doesn't mention your model or a link to nutrition / pheromones. The abstract mentions melanic gene frequencies, which I'd guess would be the genes / mutations mentioned on wikipedia. Therefore, at least the abstract agrees with the usual notion that it is a mutation that is causing the color change, and not nutrition / pheromones.
                                 
                                JK: Feeding the moth larvae a diet of leaves containing increased amount of lead and manganese caused the nutrient-dependent color change. Epistasis was achieved via the nutrient-dependent pheromone production of the female moth, which causes the observed patterns of migration (2km per night). The male moths selected for pheromones that signal nutrient-dependent reproductive fitness.  I've already mentioned this, and you continue to ignore biological facts. You want predators (birds eating the moths) to cause what is statistically represented as natural selection.

                                Leif Ekblad: 
                                 It is possible that the color chage is related to a toxic diet rather than predation, but then I never claimed anything about what drove natural selection, only how the color is coded (through a DNA mutation, not epigenetics, nutrition or pheromones).

                                JK: You cannot seem to grasp the obvious fact that gene frequencies are epigenetically effected (e.g., they are nutrient-dependent and pheromone-controlled), which is what I have detailed.

                                You wrote: Forth, there is no need for a back-mutation as all that needs to happen is new selection on the light phenotype which will increase its frequency.

                                In your world of forward and reversemoth color change, is new selection automagical? Or is "a miracle" all that needs to happen for new selection to occur?  Automagical or miraculous selection equates well with the random mutations explanation, where a mutation occurs that causes the color change, but "...there is no need for a back-mutation as all that needs to happen is new selection on the light phenotype..."

                                Do you realize how ridiculous that makes you seem to be? It's as if you would rather draw from a ridiculous theory and explain color regression via statements that are even more ridiculous. Simply put, it's as if you were Edgar Owen or Clarence 'Sonny' Williams. Perhaps they can help you form a research team to also explain eye regression in blind "cave" fish, using the same ridiculous theory as the one where you claim there is no need for "back-mutation."
                                 
                                James V. Kohl
                                Medical laboratory scientist (ASCP)
                                Independent researcher
                                Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.

                                 
                                 
                                 
                                 
                              • james kohl
                                From: Edgar Owen Kohl continually cites published works as support for his model when they actually do nothing of the sort. This is one
                                Message 15 of 21 , Apr 1, 2013
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                                  From: Edgar Owen <edgarowen@...>
                                  Kohl continually 'cites' published works as support for his 'model' when they actually do nothing of the sort. 

                                  This is one of the several ways he's fraudulently bootstrapped his reputation out of nothing....

                                  JK: My reputation includes a publication history with awards for publishing in neuroscience and social science, as well as what may be the first published work to mention molecular epigenetics in the context of behavioral development: From fertilization to adult sexual behavior. Obviously, the recently published paper on the moths has not been available for me to cite, but it is equally obvious that I will cite it in my next published work.

                                  Edgar's claim: "...he's fraudulently bootstrapped his reputation out of nothing...." is simply another libelous claim from someone who has established his ignorance of facts.

                                  James V. Kohl
                                  Medical laboratory scientist (ASCP)
                                  Independent researcher
                                  Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.



                                  On Apr 1, 2013, at 6:35 AM, Leif Ekblad wrote:

                                   

                                  

                                  JK: According to the latest research The peppered moth and industrial melanism: evolution of a natural selection case study, your reliance on wikipedia makes no sense.
                                   
                                  Leif Ekblad: The abstract doesn't mention your model or a link to nutrition / pheromones. The abstract mentions melanic gene frequencies, which I'd guess would be the genes / mutations mentioned on wikipedia. Therefore, at least the abstract agrees with the usual notion that it is a mutation that is causing the color change, and not nutrition / pheromones.
                                   
                                  JK: Feeding the moth larvae a diet of leaves containing increased amount of lead and manganese caused the nutrient-dependent color change. Epistasis was achieved via the nutrient-dependent pheromone production of the female moth, which causes the observed patterns of migration (2km per night). The male moths selected for pheromones that signal nutrient-dependent reproductive fitness.  I've already mentioned this, and you continue to ignore biological facts. You want predators (birds eating the moths) to cause what is statistically represented as natural selection.
                                  Leif Ekblad:  It is possible that the color chage is related to a toxic diet rather than predation, but then I never claimed anything about what drove natural selection, only how the color is coded (through a DNA mutation, not epigenetics, nutrition or pheromones).
                                   
                                   
                                   


                                • Leif Ekblad
                                  Leif Ekblad: It is possible that the color chage is related to a toxic diet rather than predation, but then I never claimed anything about what drove natural
                                  Message 16 of 21 , Apr 1, 2013
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                                    Leif Ekblad:  It is possible that the color chage is related to a toxic diet rather than predation, but then I never claimed anything about what drove natural selection, only how the color is coded (through a DNA mutation, not epigenetics, nutrition or pheromones).

                                    JK: You cannot seem to grasp the obvious fact that gene frequencies are epigenetically effected (e.g., they are nutrient-dependent and pheromone-controlled), which is what I have detailed.
                                    Leif Ekblad:  I know of no model that could explain that gene frequencies are related to epigenetics. The conventional knowledge of epigenetics is that it can affect gene expression, but there is no evidence that it directly can affect gene frequencies itself. If you know of any such published research, please cite it. And we have already concluded, based on both wikipedia and the Nature article, that coloration is genetic (DNA mutation), and not epigenetic. If you have issues with that, cite relevant, published, research that says otherwise.
                                     
                                    JK: In your world of forward and reversemoth color change, is new selection automagical?
                                     
                                    Leif Ekblad:  Are you telling me that you don't know about natural selection? That's what the wikipedia article is all about, and what the Nature article you cited is about as well. It's about a case of natural selection, not nutrition or pheromones like you want us to believe. When the darker phenotype becomes advantageous due to pollution, it gets an selective advantage and increases in frequency. When things go back to normal, the lighter phenotype once more becomes advantageous and increases in frequency. The actual cause for the selective advantage (predation, toxicity or something else) doesn't matter in the context of natural selection. If you don't understand basic natural selection you really shouldn't publish anything on that topic!
                                     
                                  • james kohl
                                    Leif Ekblad wrote: When the darker phenotype becomes advantageous due to pollution, it gets an selective advantage and increases in frequency. When things go
                                    Message 17 of 21 , Apr 1, 2013
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                                      Leif Ekblad wrote: When the darker phenotype becomes advantageous due to pollution, it gets an selective advantage and increases in frequency. When things go back to normal, the lighter phenotype once more becomes advantageous and increases in frequency. The actual cause for the selective advantage (predation, toxicity or something else) doesn't matter in the context of natural selection.

                                      JK: Leif just described what's called the heterozygote advantage, which is a statistical representation. It is not based on any biological facts, and it has nothing to do with Darwinian natural selection for beak morphology in finches; the head crest in pigeons or any other visually perceived phenotypic variation because Darwin clearly stated that "conditions of existence" must precede Natural Selection both in importance and when attempting to determine cause and effect.

                                      "Conditions of existence" are nutrient-dependent and pheromone-controlled.  What kind of idiot tells the group that the actual cause for the selective advantage does not matter in the context of natural selection? That was a rhetorical question. Nutrient uptake provides the advantage which is controlled by the metabolism of nutrients to species-specific pheromones that control reproduction and signal reproductive fitness in species that sexually reproduce.
                                       
                                      James V. Kohl
                                      Medical laboratory scientist (ASCP)
                                      Independent researcher
                                      Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.



                                      From: Leif Ekblad <leif@...>
                                      To: evolutionary-psychology@yahoogroups.com
                                      Sent: Mon, April 1, 2013 4:17:45 PM
                                      Subject: Re: [evol-psych] The truth about RANDOM MUTATIONS.

                                       

                                      

                                      Leif Ekblad:  It is possible that the color chage is related to a toxic diet rather than predation, but then I never claimed anything about what drove natural selection, only how the color is coded (through a DNA mutation, not epigenetics, nutrition or pheromones).

                                      JK: You cannot seem to grasp the obvious fact that gene frequencies are epigenetically effected (e.g., they are nutrient-dependent and pheromone-controlled), which is what I have detailed.
                                      Leif Ekblad:  I know of no model that could explain that gene frequencies are related to epigenetics. The conventional knowledge of epigenetics is that it can affect gene expression, but there is no evidence that it directly can affect gene frequencies itself. If you know of any such published research, please cite it. And we have already concluded, based on both wikipedia and the Nature article, that coloration is genetic (DNA mutation), and not epigenetic. If you have issues with that, cite relevant, published, research that says otherwise.
                                       
                                      JK: In your world of forward and reversemoth color change, is new selection automagical?
                                       
                                      Leif Ekblad:  Are you telling me that you don't know about natural selection? That's what the wikipedia article is all about, and what the Nature article you cited is about as well. It's about a case of natural selection, not nutrition or pheromones like you want us to believe. When the darker phenotype becomes advantageous due to pollution, it gets an selective advantage and increases in frequency. When things go back to normal, the lighter phenotype once more becomes advantageous and increases in frequency. The actual cause for the selective advantage (predation, toxicity or something else) doesn't matter in the context of natural selection. If you don't understand basic natural selection you really shouldn't publish anything on that topic!
                                       
                                    • James Gray
                                      Leif, I do hope you keep up the challenge to Kohl and that you are not intimidated by his nasty words. By now it is fairly apparent that Kohl is not a very
                                      Message 18 of 21 , Apr 1, 2013
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                                        Leif,  I do hope you keep up the challenge to Kohl and that you are not intimidated by his nasty words.  By now it is fairly apparent that Kohl is not a very nice person.  He seems able to write very clearly when he is insulting people.  His other writing is typically very unclear.  I am sure that he will hurl insults at me because of this reply.  However, he insults me even if I do not reply to him.  Any educated person will know that you were not writing about the heterozygote advantage.

                                        James Gray


                                        On Mon, Apr 1, 2013 at 4:47 PM, james kohl <jvkohl@...> wrote:
                                         

                                        Leif Ekblad wrote: When the darker phenotype becomes advantageous due to pollution, it gets an selective advantage and increases in frequency. When things go back to normal, the lighter phenotype once more becomes advantageous and increases in frequency. The actual cause for the selective advantage (predation, toxicity or something else) doesn't matter in the context of natural selection.

                                        JK: Leif just described what's called the heterozygote advantage, which is a statistical representation. It is not based on any biological facts, and it has nothing to do with Darwinian natural selection for beak morphology in finches; the head crest in pigeons or any other visually perceived phenotypic variation because Darwin clearly stated that "conditions of existence" must precede Natural Selection both in importance and when attempting to determine cause and effect.

                                        "Conditions of existence" are nutrient-dependent and pheromone-controlled.  What kind of idiot tells the group that the actual cause for the selective advantage does not matter in the context of natural selection? That was a rhetorical question. Nutrient uptake provides the advantage which is controlled by the metabolism of nutrients to species-specific pheromones that control reproduction and signal reproductive fitness in species that sexually reproduce.
                                         
                                        James V. Kohl
                                        Medical laboratory scientist (ASCP)
                                        Independent researcher
                                        Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.



                                        From: Leif Ekblad <leif@...>
                                        To: evolutionary-psychology@yahoogroups.com
                                        Sent: Mon, April 1, 2013 4:17:45 PM
                                        Subject: Re: [evol-psych] The truth about RANDOM MUTATIONS.

                                         

                                        Leif Ekblad:  It is possible that the color chage is related to a toxic diet rather than predation, but then I never claimed anything about what drove natural selection, only how the color is coded (through a DNA mutation, not epigenetics, nutrition or pheromones).

                                        JK: You cannot seem to grasp the obvious fact that gene frequencies are epigenetically effected (e.g., they are nutrient-dependent and pheromone-controlled), which is what I have detailed.
                                        Leif Ekblad:  I know of no model that could explain that gene frequencies are related to epigenetics. The conventional knowledge of epigenetics is that it can affect gene expression, but there is no evidence that it directly can affect gene frequencies itself. If you know of any such published research, please cite it. And we have already concluded, based on both wikipedia and the Nature article, that coloration is genetic (DNA mutation), and not epigenetic. If you have issues with that, cite relevant, published, research that says otherwise.
                                         
                                        JK: In your world of forward and reversemoth color change, is new selection automagical?
                                         
                                        Leif Ekblad:  Are you telling me that you don't know about natural selection? That's what the wikipedia article is all about, and what the Nature article you cited is about as well. It's about a case of natural selection, not nutrition or pheromones like you want us to believe. When the darker phenotype becomes advantageous due to pollution, it gets an selective advantage and increases in frequency. When things go back to normal, the lighter phenotype once more becomes advantageous and increases in frequency. The actual cause for the selective advantage (predation, toxicity or something else) doesn't matter in the context of natural selection. If you don't understand basic natural selection you really shouldn't publish anything on that topic!
                                         


                                      • james kohl
                                        From: James Gray Leif, I do hope you keep up the challenge to Kohl and that you are not intimidated by his nasty words. By now it is fairly
                                        Message 19 of 21 , Apr 2, 2013
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                                          From: James Gray <James@...>
                                          Leif,  I do hope you keep up the challenge to Kohl and that you are not intimidated by his nasty words.  By now it is fairly apparent that Kohl is not a very nice person.  He seems able to write very clearly when he is insulting people.  His other writing is typically very unclear.  I am sure that he will hurl insults at me because of this reply.  However, he insults me even if I do not reply to him.  Any educated person will know that you were not writing about the heterozygote advantage.

                                          JK: Leif Ekblad wrote: "When the darker phenotype becomes advantageous..." See, for example:

                                          The peppered moth and industrial melanism: evolution of a natural ...

                                          by LM Cook - 2012 - Related articles
                                          Dec 5, 2012 – The peppered moth and industrial melanism: evolution of a natural ... The possible existence and origin of heterozygote advantage has been ...

                                          If Leif was not writing about the heterozygote advantage in moths, what was he writing about?

                                          James V. Kohl
                                          Medical laboratory scientist (ASCP)
                                          Independent researcher
                                          Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.


                                          On Mon, Apr 1, 2013 at 4:47 PM, james kohl <jvkohl@...> wrote:
                                           

                                          Leif Ekblad wrote: When the darker phenotype becomes advantageous due to pollution, it gets an selective advantage and increases in frequency. When things go back to normal, the lighter phenotype once more becomes advantageous and increases in frequency. The actual cause for the selective advantage (predation, toxicity or something else) doesn't matter in the context of natural selection.

                                          JK: Leif just described what's called the heterozygote advantage, which is a statistical representation. It is not based on any biological facts, and it has nothing to do with Darwinian natural selection for beak morphology in finches; the head crest in pigeons or any other visually perceived phenotypic variation because Darwin clearly stated that "conditions of existence" must precede Natural Selection both in importance and when attempting to determine cause and effect.

                                          "Conditions of existence" are nutrient-dependent and pheromone-controlled.  What kind of idiot tells the group that the actual cause for the selective advantage does not matter in the context of natural selection? That was a rhetorical question. Nutrient uptake provides the advantage which is controlled by the metabolism of nutrients to species-specific pheromones that control reproduction and signal reproductive fitness in species that sexually reproduce.
                                           
                                          James V. Kohl
                                          Medical laboratory scientist (ASCP)
                                          Independent researcher
                                          Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.



                                          From: Leif Ekblad <leif@...>
                                          To: evolutionary-psychology@yahoogroups.com
                                          Sent: Mon, April 1, 2013 4:17:45 PM
                                          Subject: Re: [evol-psych] The truth about RANDOM MUTATIONS.

                                           

                                          Leif Ekblad:  It is possible that the color chage is related to a toxic diet rather than predation, but then I never claimed anything about what drove natural selection, only how the color is coded (through a DNA mutation, not epigenetics, nutrition or pheromones).

                                          JK: You cannot seem to grasp the obvious fact that gene frequencies are epigenetically effected (e.g., they are nutrient-dependent and pheromone-controlled), which is what I have detailed.
                                          Leif Ekblad:  I know of no model that could explain that gene frequencies are related to epigenetics. The conventional knowledge of epigenetics is that it can affect gene expression, but there is no evidence that it directly can affect gene frequencies itself. If you know of any such published research, please cite it. And we have already concluded, based on both wikipedia and the Nature article, that coloration is genetic (DNA mutation), and not epigenetic. If you have issues with that, cite relevant, published, research that says otherwise.
                                           
                                          JK: In your world of forward and reversemoth color change, is new selection automagical?
                                           
                                          Leif Ekblad:  Are you telling me that you don't know about natural selection? That's what the wikipedia article is all about, and what the Nature article you cited is about as well. It's about a case of natural selection, not nutrition or pheromones like you want us to believe. When the darker phenotype becomes advantageous due to pollution, it gets an selective advantage and increases in frequency. When things go back to normal, the lighter phenotype once more becomes advantageous and increases in frequency. The actual cause for the selective advantage (predation, toxicity or something else) doesn't matter in the context of natural selection. If you don't understand basic natural selection you really shouldn't publish anything on that topic!
                                           


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