Nov 28, 2013 by Marie Daniels
Excerpt: “We found that brain size variations are associated with changes in gene number in a large proportion of families of closely related genes. These gene families are preferentially involved in cell communication and cell movement as well as immune functions and are prominently expressed in the human brain. Our results suggest that changes in gene family size may have contributed to the evolution of larger brains in mammals.”
My comment: Cell communication, cell movement, and immune functions are nutrient-dependent. In species from microbes to man the metabolism of nutrients to species-specific pheromones controls the physiology of reproduction. Thus, brain size is a function of nutrient-dependent pheromone-controlled niche construction that starts with ecological and social niche construction that leads to neurogenic and socio-cognitive niche construction in a continuum of adaptations to the sensory environment that facilitate survival of species and their diversification. The diversiification of brain size is nutrient-dependent and pheromone-controlled.
Journal article conclusion: “…variations in GFS associated with encephalization provided an evolutionary support for the specific cellular, physiological and developmental demands associated with increased brain size in mammals.”
If “Big Brains Are All in the Genes” was an appropriate title, variations would not merely be associated with what most people know are epigenetic effects of the sensory environment on biophysically constrained specific cellular, physiological, and developmental changes that link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man via conserved molecular mechanisms. Thus, what’s represented in the journal article, and more explicitly in the journalist’s report is akin to “Evolution for Dummies” in which genes are determinants of brain size, albeit outside the context of olfactory/pheromonal input that alters ecological, social, neurogenic, and socio-cognitive niche construction. For comparison to an accurate representation of organismal complexity specific to the brain in primates, see: MicroRNA-Driven Developmental Remodeling in the Brain Distinguishes Humans from Other Primates
Epigenetically-effected tissue-specific changes in the expression of trans-regulators, such as microRNA, rather than sequence changes in cis-regulatory regions, are the driving force underlying developmental remodeling across hundreds of genes. Thus, big brains are not all in the genes. If anything was all in the genes, it would not involve remodeling due to changes in the microRNA/messenger RNA balance that result in difference in human and non-human primate brains, insect brains, and in nematode neurogenic niche construction. See also: Primate Transcript and Protein Expression Levels Evolve Under Compensatory Selection Pressures.
The compensatory selection pressures are, of course, nutrient-dependent and pheromone-controlled.
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.