“The evolution of human intellect: Human-specific regulation of neuronal genes.” November 20th, 2012.
Excerpt: “This phenomenon of “chromatin looping” is implicated in controlling the expression of neighboring genes, including several with a critical role for human brain development.”
My comment: “Chromatin looping” is nutrient chemical-dependent and controlled by species-specific pheromones. The bottom-up epigenetic effect of nutrient chemicals on the microRNA / messenger RNA balance must be controlled by the top-down epigenetic effect of pheromones to achieve intracellular homeostasis and organism-level homeostasis after its alteration by variations in the ecological niche and social niche.
Variations in the ecological niche and social niche are responsible for adaptive evolution via their epigenetic effects on intracellular signaling and intermolecular changes in DNA that lead to stochastic de novo gene expression. The ability to find nutrient chemicals varies in the ecological niche, and the ability to metabolize them to species-specific pheromones controls the social niche. Stress effects enter the complex systems biology of adaptive evolution via difficulties finding food, or difficulties interacting with conspecifics who are typically competing for the food.
For example, ingested plant microRNAs appear to influence gene expression across kingdoms, and the gene expression is controlled by messenger RNA. This epigenetically links what mammals eat to intermolecular changes, stochastic gene expression, and to new genes required for the evolutionary development of the mammalian placenta and the human brain.
In species from microbes to man, it is clear that the epigenetic effects of glucose are essential to regulating species-specific pheromone production. In mammals, glucose epigenetically effects secretion of gonadotropin releasing hormone (GnRH), which is also epigenetically effected by mammalian pheromones.
This allows nutrient chemical-dependent adaptive evolution to be controlled by the epigenetic effects of pheromones as occurs in every other species.
The article that is briefly detailed in the press release linked above is available for free here: Human-Specific Histone Methylation Signatures at Transcription Start Sites in Prefrontal Neurons. The authors clearly represent the molecular mechanisms of adaptive evolution common to all species, but they do not state clearly that they are doing so. They raise “…the intriguing possibility that coordinated epigenetic regulation via newly derived chromatin features at gene transcription start sites could play an important role in the emergence of human-specific gene expression networks in the brain.
Clearly, their focus is on primates “…and other mammals with complex social and cognitive-emotional skill sets.” But if they were to examine insect species they would undoubtedly find evidence for precisely the same epigenetic tweaking of immense gene networks in superorganisms that solve problems through the exchange and the selective cancellation and modification of signals.
Glucose
Some people will nevertheless be able to grasp their conceptualization of how single nucleotide alterations and polymorphisms contribute to uniquely human susceptibility to neurological and psychiatric disorders, for example via SLC2A3 encoding a neuronal glucose transporter linked to dyslexia and attention-deficit hyperactivity disorder or via the neuronal migration gene TUBB2B that has been linked to polymicrogria and defective neurodevelopment.
The common molecular biology of species from microbes to man make it clear that glucose is essential to the advent of sexual reproduction in yeast that signal sex difference via the alpha-mating pheromone. Glucose is also essential to nutrient chemical-dependent sexual reproduction in mammals via its epigenetic effects on intracellular signaling and secretion of GnRH, which is epigenetically effected by mammalian pheromones. The epigenetic effects of nutrient chemicals and pheromones control adaptive the evolution of primates via their effects on the GnRH neuronal system as I have detailed using the honeybee model organism to link species from microbes to man via their common molecular biology and epigenetic effects of nutrient chemicals and pheromones.
Ecological selection as the cause and sexual differentiation as the consequence of species divergence? is a free full text representation of the importance of nutrient chemicals and pheromones to concurrently controlled adaptive evolution of the mandibles and male genitalia of an insect species. As has been detailed in the honeybee model organism, this concurrent control must be due to the epigenetic tweaking of immense gene networks, or these species differences could not have adaptively evolved. So far as I know, and despite previous evidence suggesting that sexual selection is the primary driver of species divergence, these researchers provide evidence that ecological divergence precedes sexual divergence. That evidence links nutrient chemical uptake to sexual divergence in species from microbes to man.
James V. Kohl detailedl how quantized energy-dependent microRNA biogenesis links the pheromone-controlled physiology of reproduction to biophysically constrained viral latency and healthy longevity. Links from what organisms eat to the enzyme-dependent metabolism of food also link metabolic networks to microRNA-mediated genetic networks in the context of RNA interference. Drug therapies alter RNA interference by altering cell type differentiation in all cells of all individuals of all species. For comparison, during the past 26 years, Kohl has detailed how the chemistry of protein folding is biophysically constrained at every level of biological organization by conserved molecular mechanisms.