Epigenetic regulation of puberty via Zinc finger protein-mediated transcriptional repression

Reported as:

Researchers elucidate network of genes that control when puberty begins

Excerpt:

…have identified for the first time members of an elaborate superfamily of genes that regulate the timing of puberty in highly evolved nonhuman primates.

My comment: Who do these researches and science journalists think they are fooling when they report the nutrient-dependent pheromone-controlled onset of puberty, which is obviously RNA-mediated, in the context of highly evolved organisms? No experimental evidence of biologically-based cause and effect links evolution and puberty.

Conserved molecular mechanisms of biophysically constrained cell type differentiation link protein folding chemistry from thermodynamic cycles of nutrient-dependent protein biosynthesis and degradation to the stability of all organized genomes via microRNAs, cell adhesion proteins, and supercoiled DNA. Networks of genes link metabolism to survival of cell types and species via the metabolic networks and genetic networks that control organism-level thermoregulation.

A single nutrient-dependent RNA-mediated amino acid substitution in a virus links energy theft from cells to perturbed protein folding and mutation-driven pathology. That explains why PKU was linked from nutritional epigenetics to pharmocogenomics several decades ago and why nutrient-dependent base pair substitutions and RNA-mediated cell type differentiation was linked to human life history transitions by the Val158Met substitution last year.

See: Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults

There is no explanation for the ignorance of evolutionary theorists who claim that Zinc finger protein-mediated transcriptional repression can be placed into the context of the evolution of puberty. Nothing currently known about RNA-mediated cell type differentiation can be placed into the context of evolution. Everything  known to serious scientists has been placed into the context of ecological variation and ecological adaptation.

See: Distinct E-cadherin-based complexes regulate cell behaviour through miRNA processing or Src and p120 catenin activity

My comment: Everything  known to serious scientists also supports our claims about Zinc finger proteins from the “Genetic Considerations” section of our 1996 Hormones and Behavior review From Fertilization to Adult Sexual Behavior

Excerpt:

Another example of biological sex differences which are neither gonadal nor hormonal, however, is provided by the homologous but dimorphic zinc finger proteins ZFX and ZFY encoded on the X and Y chromosomes (North et al.,1991). An early study of human expression of ZFX and ZFY reported different transcript sizes from the two genes and this difference was even apparent in somatic tissues (Page, Disteche, Simpson, De La Chapelle, Andersson, Alitalo, Brown, Green, and Akots, 1990). ZFX and ZFY are described as “DNA-binding proteins” and via their binding of sexually dimorphic proteins, chromatin structure and transcription could be modulated in sexually dimorphic ways as a result of females having only ZFX binding events, whereas males would have a mixture of both ZFX and ZFY binding events (Fiddler, Abdel-Rahman, Rappolee, and Pergament, 1995; Lau and Chan, 1989; Zwingman, Erickson, Boyer, and Ao, 1995).

My comment: Any report that links sex differences in cell types to somatic differences in cell types and claims that the differences exemplify how evolution has altered life history transitions in highly evolved primates exemplifies the amount of pseudoscientific nonsense about hormone-organization and hormone-activation that has continued to be taught to researchers and science journalists.

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