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[evol-psych] Re: [human-ethology] Functional potential of genes: Pushing the boundaries of transcription

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  • anonymous_9001
    ... Compared to the generic excerpt from your paper that you copy and paste all the time as an answer to everything? ... Considering those processes can be
    Message 1 of 15 , May 12, 2013
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      --- In evolutionary-psychology@yahoogroups.com, james kohl <jvkohl@...> wrote:

      > JK: Thanks for making this clear. What you think is an answer to my question is
      > citations to book length works or wiki representations.


      Compared to the generic excerpt from your paper that you copy and paste all the time as an answer to everything?


      >For example, the wiki
      > representation is that "Genome size can increase by duplication, insertion, or
      > polyploidation.' Are those examples of mechanisms you would like to compare to
      > the molecular mechanisms that are nutrient-dependent and pheromone controlled
      > via epigenetic effects on intracellular signaling, intermolecular interactions,
      > stochastic gene expression et al.? Or, are duplication, insertion, and
      > polyploidation nutrient-dependent and pheromone-controlled?


      Considering those processes can be observed in vitro, not necessarily.

      http://www.pnas.org/content/86/23/9253.full.pdf
      http://www.nature.com/ng/journal/v40/n3/abs/ng.f.94.html


      > I'm saying that the epigenetic effects of nutrients and pheromones alter
      > duplication, insertion, and polyploidation, and you're telling everyone that I'm
      > not answering your questions.


      What effects specifically? What nutrients or pheromones induce polyploidization through what mechanism? What nutrients or pheromones trigger transposable elements and how?
    • james kohl
      This will be my last communication on this topic with anonymous_9001 because of my frustration with the scientificilliteracy I have encountered (see below). It
      Message 2 of 15 , May 12, 2013
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        This will be my last communication on this topic with anonymous_9001 because of my frustration with the scientific illiteracy I have encountered (see below). It is simply not possible to explain how the epigenetic landscape becomes the physical landscape of DNA to someone who will not indicate what processes they think are involved, so that those processes can be compared to the ones I have detailed in species from microbes to man.

        It would be helpful if others also tell me how they think
        the epigenetic landscape becomes the physical landscape of DNA before telling me that my details of this are wrong. For example, see:

        Regulated Noise in the Epigenetic Landscape of Development and Disease

        "Stochastic Noise, Buffering, and Epigenetic Modulation of Phenotypic Plasticity
        "
        Cell individuality was first observed in bacteria in 1976 (Spudich and Koshland, 1976) and has been implicated in generating behavioral variability, as well as determining cell fate, ever since (Korobkova et al., 2004; Maamar et al., 2007; Rao et al., 2002). Many of these observations have also found support in mammalian systems, and there are now many examples of the important role that noise plays in cell fate decisions in organisms ranging from bacteria to humans (Losick and Desplan, 2008)."

        Tell us how they misrepresent cause and effect, and then move forward to tell me how I have misrepresented it in: Nutrient-dependent / Pheromone-controlled Adaptive Evolution
        Nutrient-dependent / Pheromone-controlled thermodynamics and thermoregulation
        Clearly, if the functional potential of genes is not nutrient-dependent and pheromone-controlled, someone must propose an alternative that is not automagical. If you don't like the details of my model, attempt to explain how non-olfactory/pheromonal sensory input from the environment might somehow be responsible for adaptive evolution. Then, when you fail to explain anything at all, we can discuss what I have detailed. Until then, anonymous and others should simple consider themselves to be too under-informed to enter discussion of biological 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.



        From: anonymous_9001 <anonymous_9001@...>
        To: evolutionary-psychology@yahoogroups.com
        Sent: Sun, May 12, 2013 12:55:52 PM
        Subject: [evol-psych] Re: [human-ethology] Functional potential of genes: Pushing the boundaries of transcription

         



        --- In evolutionary-psychology@yahoogroups.com, james kohl <jvkohl@...> wrote:

        > JK: Thanks for making this clear. What you think is an answer to my question is
        > citations to book length works or wiki representations.

        Compared to the generic excerpt from your paper that you copy and paste all the time as an answer to everything?

        >For example, the wiki
        > representation is that "Genome size can increase by duplication, insertion, or
        > polyploidation.' Are those examples of mechanisms you would like to compare to
        > the molecular mechanisms that are nutrient-dependent and pheromone controlled
        > via epigenetic effects on intracellular signaling, intermolecular interactions,
        > stochastic gene expression et al.? Or, are duplication, insertion, and
        > polyploidation nutrient-dependent and pheromone-controlled?

        Considering those processes can be observed in vitro, not necessarily.

        http://www.pnas.org/content/86/23/9253.full.pdf
        http://www.nature.com/ng/journal/v40/n3/abs/ng.f.94.html

        > I'm saying that the epigenetic effects of nutrients and pheromones alter
        > duplication, insertion, and polyploidation, and you're telling everyone that I'm
        > not answering your questions.

        What effects specifically? What nutrients or pheromones induce polyploidization through what mechanism? What nutrients or pheromones trigger transposable elements and how?

      • anonymous_9001
        I have given you links describing molecular processes involved in modifying the genome. You have given me a bunch of unrelated nonsense. The Pujadas paper does
        Message 3 of 15 , May 12, 2013
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          I have given you links describing molecular processes involved in modifying the genome. You have given me a bunch of unrelated nonsense. The Pujadas paper does not address how changes to the genome are made. It describes how stochastic processes produce phenotypic variation. That is not what I'm asking about, so stop changing the subject.

          You have refused to answer the simple question: What molecular processes make changes to the genome in your model? I've read your paper. You make no mention of pathways, enzymes, or anything else of that sort that deals with the genome.


          --- In evolutionary-psychology@yahoogroups.com, james kohl <jvkohl@...> wrote:
          >
          > This will be my last communication on this topic with anonymous_9001 because of
          > my frustration with the scientificilliteracy I have encountered (see below). It
          > is simply not possible to explain how the epigenetic landscape becomes the
          > physical landscape of DNA to someone who will not indicate what processes they
          > think are involved, so that those processes can be compared to the ones I have
          > detailed in species from microbes to man.
          >
          >
          > It would be helpful if others also tell me how they think the epigenetic
          > landscape becomes the physical landscape of DNA before telling me that my
          > details of this are wrong. For example, see:
          >
          > Regulated Noise in the Epigenetic Landscape of Development and Disease
          >
          > "Stochastic Noise, Buffering, and Epigenetic Modulationof Phenotypic Plasticity"
          > Cell individuality was first observed in bacteria in 1976 (Spudich and Koshland,
          > 1976) and has been implicated in generating behavioral variability, as well as
          > determining cell fate, ever since (Korobkova et al., 2004; Maamar et al., 2007;
          > Rao et al., 2002). Many of these observations have also found support in
          > mammalian systems, and there are now many examples of the important role that
          > noise plays in cell fate decisions in organisms ranging from bacteria to humans
          > (Losick and Desplan, 2008)."
          >
          > Tell us how they misrepresent cause and effect, and then move forward to tell me
          > how I have misrepresented it in: Nutrient-dependent / Pheromone-controlled
          > Adaptive Evolution
          > Nutrient-dependent / Pheromone-controlled thermodynamics and thermoregulation
          > Clearly, if the functional potential of genes is not nutrient-dependent and
          > pheromone-controlled, someone must propose an alternative that is not
          > automagical. If you don't like the details of my model, attempt to explain how
          > non-olfactory/pheromonal sensory input from the environment might somehow be
          > responsible for adaptive evolution. Then, when you fail to explain anything at
          > all, we can discuss what I have detailed. Until then, anonymous and others
          > should simple consider themselves to be too under-informed to enter discussion
          > of biological 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.
        • Leif Ekblad
          Yes, exactly my opinion. He talks about the honeybee model that is similar to genders in mammals as if it could explain everything. But the truth of course is
          Message 4 of 15 , May 13, 2013
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            Yes, exactly my opinion. He talks about the honeybee model that is similar
            to genders in mammals as if it could explain everything. But the truth of
            course is that all the phenotypes of honeybees are coded in DNA, just like
            gender is in animals, and that these are then turned on during development.
            This has nothing to do with evolution as he cannot explain how the
            phenotypes created by epigenetics are feed back into the germ line as novel
            DNA. To use his own words, what would be the model for that? He hasn't
            explained that in any of his papers that I've read, and none of them talks
            about this because such claims would have been rejected as nonsense by
            peer-reviewers.

            Leif Ekblad


            ----- Original Message -----
            From: "anonymous_9001" <anonymous_9001@...>
            To: <evolutionary-psychology@yahoogroups.com>
            Sent: Monday, May 13, 2013 3:12 AM
            Subject: [evol-psych] Re: [human-ethology] Functional potential of genes:
            Pushing the boundaries of transcription


            >I have given you links describing molecular processes involved in modifying
            >the genome. You have given me a bunch of unrelated nonsense. The Pujadas
            >paper does not address how changes to the genome are made. It describes how
            >stochastic processes produce phenotypic variation. That is not what I'm
            >asking about, so stop changing the subject.
            >
            > You have refused to answer the simple question: What molecular processes
            > make changes to the genome in your model? I've read your paper. You make
            > no mention of pathways, enzymes, or anything else of that sort that deals
            > with the genome.
            >
            >
            > --- In evolutionary-psychology@yahoogroups.com, james kohl <jvkohl@...>
            > wrote:
            >>
            >> This will be my last communication on this topic with anonymous_9001
            >> because of
            >> my frustration with the scientificilliteracy I have encountered (see
            >> below). It
            >> is simply not possible to explain how the epigenetic landscape becomes
            >> the
            >> physical landscape of DNA to someone who will not indicate what processes
            >> they
            >> think are involved, so that those processes can be compared to the ones I
            >> have
            >> detailed in species from microbes to man.
            >>
            >>
            >> It would be helpful if others also tell me how they think the epigenetic
            >> landscape becomes the physical landscape of DNA before telling me that my
            >> details of this are wrong. For example, see:
            >>
            >> Regulated Noise in the Epigenetic Landscape of Development and Disease
            >>
            >> "Stochastic Noise, Buffering, and Epigenetic Modulationof Phenotypic
            >> Plasticity"
            >> Cell individuality was first observed in bacteria in 1976 (Spudich and
            >> Koshland,
            >> 1976) and has been implicated in generating behavioral variability, as
            >> well as
            >> determining cell fate, ever since (Korobkova et al., 2004; Maamar et al.,
            >> 2007;
            >> Rao et al., 2002). Many of these observations have also found support in
            >> mammalian systems, and there are now many examples of the important role
            >> that
            >> noise plays in cell fate decisions in organisms ranging from bacteria to
            >> humans
            >> (Losick and Desplan, 2008)."
            >>
            >> Tell us how they misrepresent cause and effect, and then move forward to
            >> tell me
            >> how I have misrepresented it in: Nutrient-dependent /
            >> Pheromone-controlled
            >> Adaptive Evolution
            >> Nutrient-dependent / Pheromone-controlled thermodynamics and
            >> thermoregulation
            >> Clearly, if the functional potential of genes is not nutrient-dependent
            >> and
            >> pheromone-controlled, someone must propose an alternative that is not
            >> automagical. If you don't like the details of my model, attempt to
            >> explain how
            >> non-olfactory/pheromonal sensory input from the environment might somehow
            >> be
            >> responsible for adaptive evolution. Then, when you fail to explain
            >> anything at
            >> all, we can discuss what I have detailed. Until then, anonymous and
            >> others
            >> should simple consider themselves to be too under-informed to enter
            >> discussion
            >> of biological 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.
            >
            >
            >
            >
            >
            >
            > ------------------------------------
            >
            > Yahoo! Groups Links
            >
            >
            >
          • james kohl
            From: Leif Ekblad Yes, exactly my opinion. He talks about the honeybee model that is similar to genders in mammals as if it could explain
            Message 5 of 15 , May 13, 2013
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              From: Leif Ekblad
              Yes, exactly my opinion. He talks about the honeybee model that is similar

              to genders in mammals as if it could explain everything. But the truth of
              course is that all the phenotypes of honeybees are coded in DNA, just like
              gender is in animals, and that these are then turned on during development.
              This has nothing to do with evolution as he cannot explain how the
              phenotypes created by epigenetics are feed back into the germ line as novel
              DNA. To use his own words, what would be the model for that? He hasn't
              explained that in any of his papers that I've read, and none of them talks
              about this because such claims would have been rejected as nonsense by
              peer-reviewers.

              Leif,

              You know very well that I have two award-winning peer reviewed publications. One in Neuroendocrinology Letters and the other in the Handbook of the Evolution of Human Sexuality. What kind of idiot tells others that my "...claims would have been rejected as nonsense by
              peer-reviewers" when they obviously only rejected by those like you who are horribly under informed?

              JVK


              ----- Original Message -----
              From: "anonymous_9001" <anonymous_9001@...>
              To: <evolutionary-psychology@yahoogroups.com>
              Sent: Monday, May 13, 2013 3:12 AM
              Subject: [evol-psych] Re: [human-ethology] Functional potential of genes:
              Pushing the boundaries of transcription

              >I have given you links describing molecular processes involved in modifying
              >the genome. You have given me a bunch of unrelated nonsense. The Pujadas
              >paper does not address how changes to the genome are made. It describes how
              >stochastic processes produce phenotypic variation. That is not what I'm
              >asking about, so stop changing the subject.
              >
              > You have refused to answer the simple question: What molecular processes
              > make changes to the genome in your model? I've read your paper. You make
              > no mention of pathways, enzymes, or anything else of that sort that deals
              > with the genome.
              >
              >
              > --- In evolutionary-psychology@yahoogroups.com, james kohl
              > wrote:
              >>
              >> This will be my last communication on this topic with anonymous_9001
              >> because of
              >> my frustration with the scientificilliteracy I have encountered (see
              >> below). It
              >> is simply not possible to explain how the epigenetic landscape becomes
              >> the
              >> physical landscape of DNA to someone who will not indicate what processes
              >> they
              >> think are involved, so that those processes can be compared to the ones I
              >> have
              >> detailed in species from microbes to man.
              >>
              >>
              >> It would be helpful if others also tell me how they think the epigenetic
              >> landscape becomes the physical landscape of DNA before telling me that my
              >> details of this are wrong. For example, see:
              >>
              >> Regulated Noise in the Epigenetic Landscape of Development and Disease
              >>
              >> "Stochastic Noise, Buffering, and Epigenetic Modulationof Phenotypic
              >> Plasticity"
              >> Cell individuality was first observed in bacteria in 1976 (Spudich and
              >> Koshland,
              >> 1976) and has been implicated in generating behavioral variability, as
              >> well as
              >> determining cell fate, ever since (Korobkova et al., 2004; Maamar et al.,
              >> 2007;
              >> Rao et al., 2002). Many of these observations have also found support in
              >> mammalian systems, and there are now many examples of the important role
              >> that
              >> noise plays in cell fate decisions in organisms ranging from bacteria to
              >> humans
              >> (Losick and Desplan, 2008)."
              >>
              >> Tell us how they misrepresent cause and effect, and then move forward to
              >> tell me
              >> how I have misrepresented it in: Nutrient-dependent /
              >> Pheromone-controlled
              >> Adaptive Evolution
              >> Nutrient-dependent / Pheromone-controlled thermodynamics and
              >> thermoregulation
              >> Clearly, if the functional potential of genes is not nutrient-dependent
              >> and
              >> pheromone-controlled, someone must propose an alternative that is not
              >> automagical. If you don't like the details of my model, attempt to
              >> explain how
              >> non-olfactory/pheromonal sensory input from the environment might somehow
              >> be
              >> responsible for adaptive evolution. Then, when you fail to explain
              >> anything at
              >> all, we can discuss what I have detailed. Until then, anonymous and
              >> others
              >> should simple consider themselves to be too under-informed to enter
              >> discussion
              >> of biological 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.
              >
              >
              >
              >
              >
              >
              > ------------------------------------
              >
              > Yahoo! Groups Links
              >
              >
              >

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