Epigenetic control of female puberty and sexual orientation
January 30, 2013 | James Kohl
In case you missed it…
My comment: I attempted to add the comment below, but am not sure it will be posted to the Scientist site.
In my model, the epigenetic control of female puberty also links nutrient-dependent pheromone-controlled adaptive evolution in microbes to control of sex differences in GnRH-directed brain development and behavior in mammals. In the context of pre-pubertal GnRH-directed mammalian brain development and behavior, I tried to emphasize earlier that sex-specific regulation of miRNA levels are known to influence sexually dimorphism of mRNA. Now, there’s evidence that the Polycomb group (PcG) of transcriptional silencers (the PcG complex) represses sexual maturity “…by targeting downstream genes involved in the stimulatory control of GnRH secretion at puberty.”
That evidence takes me back to a section on molecular epigenetics in our 1996 review “From fertilization to adult sexual behavior” (with my emphasis, sans citations): “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. 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.”
Translation: Sex differences in behavior and sexual orientation are determined genetic predispositions and by nutrient chemicals and pheromones that epigenetically effect the microRNA / messenger RNA balance, intracellular signaling, and stochastic gene expression during the GnRH-driven prenatal and postnatal maturation of the brain and behavior in heterosexuals and homosexuals. While this explanation of sexual orientation is not as simple as other attempts to explain away sexual orientation, the details of how genetically predisposed differences in sexual orientation are epigenetically effected also explain the diversity of sexual behaviors observed across species and in our own.
Simply put, the molecular biology of nutrient-dependent pheromone-controlled adaptive evolution is the same in species from microbes to man. That makes the “answer to homosexuality” the same as the answer for other causality. The cause is genetically predisposed nutrient-dependent pheromone-controlled adaptive evolution. How could it not be?