Behavior (2): All responses are RNA-mediated not genetically-determined

By: James V. Kohl | Published on: September 13, 2014

Diana Maria Petrosanu also asked: “who was the author of the article that had stolen your ideas?
I cannot recall claiming that anyone had stolen our ideas or my ideas.
See: Behavior: The first response is RNA-mediated not genetically-determined. In subsequent published works, I extended what we detailed about the molecular epigenetics of sex differences in cell types from yeasts to mammals via examples from model organisms of RNA-mediated cell type differentiation in different species. That is why I was surprised to see this title: The Biological Basis of Human Sexual Orientation: Is There a Role for Epigenetics?” I’ve requested a pdf reprint of the article from Dr. Vilain. I do not expect that he cited our 1996 review because I do not recall him even mentioning any works I have authored or co-authored in his publications? Is he ignoring my past publications?
For example, in our 1996 Hormones and Behavior review we (TB) wrote: “Parenthetically it is interesting to note even the yeast Saccharomyces cerevisiae has a gene-based equivalent of sexual orientation (i.e., a-factor and alpha-factor physiologies). These differences arise from different epigenetic modifications of an otherwise identical MAT locus (Runge and Zakian, 1996; Wu and Haber, 1995).”
The connection from RNA-mediated events to epigenetic modifications of the MAT locus should have been clear to any geneticist who did not know how mutations in DNA could lead to sex differences and to sexual orientation in different cell types. However, many of those who study human sexuality are like those who study evolutionary psychology. I think that is why this question was posed: Is There a Role for Epigenetics?
Anyone taught to believe an unknown evolutionary event might someday be linked to sex differences in cell types or to any and all other cell type differences in all cells of all individuals of all species has been taught to believe in pseudoscientific nonsense, and to ignore biological facts about RNA-mediated events that we (TB) detailed 18 years ago. Those who were not taught that mutations caused sex differences in cell types may have been left to wonder about how sexual orientation somehow ‘evolved.’ That’s just speculation on my part. Some people probably weren’t taught anything and never questioned the likely role of RNA-mediated events, or never questioned their teachers who probably still know nothing about molecular epigenetics and RNA-mediated events.
We wrote: “Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans. That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.” (p. 337)
Was anyone taught to believe the truth about the molecular epigenetics of cell type differentiation in species from microbes to man? When I saw the question “Is there a role for epigenetics,” I decided to look more at what Eric Vilain was telling people about how sex differences in cell types arise. See, for examples:
Sex Differences in Brain and Behavior: Hormones Versus Genes
Excerpt: “We hypothesize that one central neuronal pathway establishes sexual attraction to either males or females, usually to the opposite sex. However, a variety of genetic and nongenetic biological effects might intersect this pathway (p. 260).”
My comment: In my model, the GnRH neuronal pathway establishes classically-conditioned sexual preferences in the context of epigenetically-effected RNA-mediated events via the same pathway that links food odors to experience-dependent classically-conditioned food preferences.
The genetics of sex differences in brain and behavior
Excerpt: “Altogether, there is mounting evidence for a genetic role of human sexual orientation. The overwhelming dominance of heterosexual behavior in the animal kingdom points at a tight molecular regulation of this trait.”
My comment: In my model, nutrient-dependent pheromone-controlled effects on RNA-mediated events tightly regulate the molecular epigenetics of this trait throughout the animal kingdom. That means that human sexual orientation, like the sexual orientation of sexually-differentiation cell types in yeasts is genetically predisposed. There may be mounting evidence for a genetic role of human sexual orientation, but I haven’t seen any of it. All I’ve seen is increasingly more evidence that sexual orientation is epigenetically-effected by sensory stimuli that cause RNA-mediated events.
The effects of perinatal testosterone exposure on the DNA methylome of the mouse brain are late-emerging
Excerpt: “…methylation patterns particularly during adulthood and that the emergence of sex differences in the brain may be a gradual process that is cemented over the organism’s life. Our data provide a new perspective by showing that most sex differences in CpG methylation are dynamic and not the result of acute modifications in response to hormones.”
My comment: I do not know why anyone ever thought that “…the emergence of sex differences in the brain…” was not “…a gradual process that is cemented over the organism’s life.” Attributing the sex differences to dynamic modifications but not acute modifications in hormones that organize and activate sex differences in behaviors,which obviously develop during life cycle transitions, may be the only accurate attribution Vilain has ever linked to RNA-mediated events that are epigenetically-effected by olfactory/pheromonal input that alters hormones that affect the behavior of all vertebrates and invertebrates via conserved molecular mechanisms.
My comment (from our 1996 review): Molecular epigenetics. It is now understood that certain genes undergo a process called “genomic or parental imprinting.” Early in embryonic development attached methyl groups become removed from most genes. Several days later, methyl groups are reattached in appropriate sites. Fascinatingly, some such genes reestablish methylation patterns based upon whether the chromosomal segment carrying the gene came from maternal or paternal chromosomes.
Although Eric Vilain and his co-authors may think their “…data provide a new perspective…” the quote from our review should make others wonder what his group thinks is a “new perspective.”  Indeed, anyone who has followed the research on epigenetically-effected RNA-mediated events and hormones that affect behavior might wonder why anyone else ever might have thought that the RNA-mediated events did not occur across the life history transitions of species from insects to mammals.
For example, I never thought I was “Born to be Wild.” But, after I started my research on human pheromones in 1982, I gradually learned to accept the fact that my behavior was epigenetically-effected by human pheromones. From 1996 until today, I have never seen any experimental evidence of biologically-based cause and effect that links anyone’s behavior to anything that is not epigenetically-effected and RNA-mediated.
For reasons that should long ago have become obvious to all others, I am now sure that all their behavior occurs in the context of ecological variation that leads from epigenetically-effected RNA-mediated differentiation of cell types by nutrient-dependent amino acid substitutions. It is the amino acid substitutions that link behaviors manifested in ecologically adapted morphological and behavioral phenotypes to conserved molecular mechanisms in species from microbes to man.

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