Loading ...
Sorry, an error occurred while loading the content.

Re: [evol-psych] RE: Genes and courtship behavior revisited

Expand Messages
  • james kohl
    Leif Ekblad wrote:  I ll soon challenge your paper on human sexual development by showing that humans have two distinct versions of courtship... The idea
    Message 1 of 4 , Sep 25, 2013
    • 0 Attachment
      Leif Ekblad wrote:  "I'll soon challenge your paper on human sexual development by showing that humans have two distinct versions of courtship..."

      "The idea that human sexual behavior only has a age and gender component is simply not correct. It also has two very different coding-schemes for how the courtship behavior is carried out."

      JK: Take your time, Leif. Challenging all that's currently known about adaptive evolution in species from microbes to man is a daunting task, even if you only include humans with ASDs as the basis of your challenge. Also, see my award-winning journal article/book chapter to ensure you challenge what is already known about human sexual development: The Mind's Eyes: Human pheromones, neuroscience, and male sexual preferences.
       
      James V. Kohl
      Medical laboratory scientist (ASCP)
      Independent researcher
      Kohl, J.V. (2013) Nutrient-dependent/pheromone-controlled adaptive evolution: a model. Socioaffective Neuroscience & Psychology, 3: 20553.
      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@..." <leif@...>
      To: evolutionary-psychology@yahoogroups.com
      Sent: Wednesday, September 25, 2013 4:16 AM
      Subject: [evol-psych] RE: Genes and courtship behavior revisited

       
      JK: When these authors add that "the sex difference in behaviour— arises at the single-cell and single-molecule levels" and that  "this picture also holds in other organisms" (e.g.,  in C. elegans, male-specific sexual attraction behavior is repressed by a single neuron pair)" and that  female mice lacking Trpc2, a pheromone-transducing channel gene, display male-type sexual behaviour, it becomes clearer why mutations theory is irrelevant to the 8-stages ofgenetically predisposed experience-dependent hormone organized and hormone activated brain development and behavior. But also, the behavioural switching associated with temperature-induced sexual transformation in reptiles and socially regulated sexual transformation in some fish reportedly may have a similar mechanistic substrate (sans mutations theory). 

      Leif Ekblad: You are once more confusing what is creating a male or female phenotype with coding of courtship behavior. It's been known for some time that male and female phenotypes are activated by hormones during development (and thus not directly controlled by genes), just as the phenotypes of honeybees are activated from nutrition (and possibly reptiles via temperature). That does not mean that the phenotypes are epigenetic, or that they don't rely on mutations. The switches that turn on phenotypes are controlling the actual genes that express things like courtship, not coding for courtship itself. Therefore, it is not interesting from an evolutionary standpoint if phenotypes can be activated via nutrition (as in honebees) or sex-hormones (as in humans), as this process doesn't describe how actual courtship is coded. To understand this you only need to consider that chimp and human have exactly the same process that determines gender (and probably exactly the same sequence that codes for the highly conserved control mechanism), yet humans and chimps don't have the same courtship behavior. And it doesn't follow that because gender is not directly coded for in DNA, the species-typical courtship behavior then must be epigenetic. That's not a valid conclusion.
       
      Besides, I'll soon challenge your paper on human sexual development by showing that humans have two distinct versions of courtship, and while you have dismissed the less common variant as disordered, I'll show it is perfectly healthy and evolutionary sound, and that it cannot possibly be epigenetic since it has a consistent form in unrelated individuals that have grown up in very different environments worldwide. The idea that human sexual behavior only has a age and gender component is simply not correct. It also has two very different coding-schemes for how the courtship behavior is carried out.

      Leif Ekblad



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

      Williams wrote: I link this review paper because it asks...and answers...the question, "How can a single gene (fru in D. melanogaster) control such an elaborate, complex behavior as male courtship?"  If you get a chance to read it, you will see how an answer can be derived without invoking genetic determinism.  Moreover, the paper is so comprehensive and wide-ranging, it could comprise a whole college-level class on development, neural circuitry and adult behavior.

      JK: The paper answers the questions about how a single gene controls male courtship by clearly stating that mutations are not involved.

      "There are, however, no signs that the M-sequence has accumulated mutations in D. melanogaster, implying that this sequence is maintained without changes."

      Feierman added: There are many (I believe hundreds) of known mutations of the SRY gene in humans that causes Androgen Insensitivity Syndrome (AIS) with rather profound effects on male courtship.

      JK: That comment is irrelevant in the context of college-level classes on development, neural circuitry and adult behaviors because no experimental evidence has ever suggested that new alleles associated with mutations are fixed in the genome.

      Williams and Feierman probably do not realize that this article is another refutation of mutation-driven evolution. It also incorporates D. melanogaster in the same context we used in our 1996 review article's section on molecular epigenetics. We wrote: "Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes..." Thus, when Williams indicates that an answer can be derived without invoking genetic determinism, he echoes the sentiments we expressed with details of cause and effect in our 1996 review.

      I'm not sure how Williams could have missed the connection to my model, given the focus of this paper on 1) the courtship-inhibiting male pheromone that 2) induces discharges in specific odorant receptor 3) expressing olfactory receptor neurons, which 4) selectively project to 5) a sexually dimorphic glomerulus 6) in the primary olfactory center, 7) where they form cholinergic synapses onto 8) projection neurons of the dopaminergic reward system. After all, these 8 stages are precisely what's predicted in my model via genetically predisposed experience-dependent hormone organized and hormone activated brain development and behavior that is epigenetically effected by olfactory/pheromonal input in vertebrates and invertebrates.

      When these authors add that "the sex difference in behaviour— arises at the single-cell and single-molecule levels" and that  "this picture also holds in other organisms" (e.g.,  in C. elegans, male-specific sexual attraction behavior is repressed by a single neuron pair)" and that  female mice lacking Trpc2, a pheromone-transducing channel gene, display male-type sexual behaviour, it becomes clearer why mutations theory is irrelevant to the 8-stages of genetically predisposed experience-dependent hormone organized and hormone activated brain development and behavior. But also, the behavioural switching associated with temperature-induced sexual transformation in reptiles and socially regulated sexual transformation in some fish reportedly may have a similar mechanistic substrate (sans mutations theory).

      What might happen if a single nutrient-dependent amino acid substitution caused a difference in the blend of pheromones produced in flies as it does in the Ostrinia moth and in humans? Here's what. It would exemplify in flies how the conserved molecular mechanisms in species from microbes to man enable nutrient-dependent pheromone-controlled adaptive evolution. It is especially interesting in flies, however, that nutrient uptake in their ecological niche is so closely related to pheromone-controlled sexual reproduction in their social niche and that they deposit their larvae where they eat and breed. 

      Now, when ever anyone like Williams or Feierman tout mutation-driven evolution, others can ask: But how could an article like this one comprise a whole college-level class on development, neural circuitry and adult behavior if mutations were involved in adaptive evolution. Besides, we know that mutations are not involved in the adaptive evolution of any species from microbes to man -- especially not in flies.
       
      James V. Kohl
      Medical laboratory scientist (ASCP)
      Independent researcher
      Kohl, J.V. (2013) Nutrient-dependent/pheromone-controlled adaptive evolution: a model. Socioaffective Neuroscience & Psychology, 3: 20553.
      Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.


    Your message has been successfully submitted and would be delivered to recipients shortly.