Neuronal copy number variation (CNV) and the brain
November 1, 2013 | James Kohl
Science 1 November 2013: Vol. 342 no. 6158 p. 577 DOI: 10.1126/science.342.6158.577
Excerpt: “This year’s neuroscience special issue is devoted to general and also several more specific aspects of research on connectivity in the brain.”
My comment (accepted for publication to the Science site on 11/4/13) : Re: Mosaic Copy Number Variation in Human Neurons.
The neuronal copy number variation (CNV) can be traced to its origins in yeasts, when epigenetically-effected CNVs enable self vs non-self recognition at the advent of immune system function and sexual reproduction, albeit sans neurons.
Olfactory/pheromonal input is subsequently associated with alternative splicings that link the epigenetic ‘landscape” to the physical landscape of DNA in the organized genome of species from microbes to man via CNVs. During adaptive evolution the CNVs in neurons are directly linked from olfactory/pheromonal input via ecological, social, neurogenic, and socio-cognitive niche construction. For example, neuronal niche construction in nematodes proceeds across species via conserved molecular mechanisms required for the thermodynamics of seemingly futile nutrient-dependent cycles of protein synthesis and degradation to species-specific pheromones. Pheromones control the physiology of reproduction and help to control nutrient-dependent organism-level thermoregulation.
In a mammal, see for example: Odorant receptor gene choice and axonal wiring in mice with deletion mutations in the odorant receptor gene SR1. However, see also my ISHE Summer Institute poster session for details that eliminate mutations from further consideration in adaptive evolution. To do that I used examples from nematodes, insects, other mammals, and a human population that arose in what is now central China during the past ~30,000 years.
Non-random experience-dependent adaptive evolution occurs due to a thermodynamically controlled single base pair change and nutrient-dependent amino acid substitution best exemplified in the mouse model via what is neuroscientifically known about nutrient-dependent pheromone-controlled reproduction.
Note: I have made four attempts to post this comment to the ISHE’s human ethology yahoo group, and the moderator, Jay Feierman, is blocking the added response to Clarence ‘Sonny’ Williams post about the special issue on neuroscience.
Within one week of science news, researchers attempting to make scientific progress have been offered the opportunity to select neuroscience or nonsense. I mention this because there is no model for the snake-centric evolution of the human brain and behavior. For contrast, every model organism on this planet attests to the fact that snake-centric evolution is the most ridiculous theory ever to be discussed among scientists or those who are scientifically illiterate evolutionary theorists. See, for example: Afraid of Snakes? Your Pulvinar May Be to Blame.
Ask what story was of most interest to any evolutionary theorist you know, and remember that theorists are probably teaching your children, grandchildren, and great-grandchildren to ignore biological facts and animal models that link the epigenetic ‘landscape’ to nutrient-dependent pheromone-controlled adaptive evolution in species from microbes to man.
This comment to the ISHE’s human ethology yahoo group was approved after the second attempt, and I will address it more thoroughly after I have acquired the reprint of the latest work from senior author Bradley Cooke.
Given your current understanding of how connections in the brain are involved in behavior, please try to put the following articles (or any articles published anywhere else in the past decade) into the context of mutation-initiated natural selection, or snake-centric evolution of the human brain via molecular mechanisms that led to visual primacy in humans.
My current understanding of receptor-mediated changes in brain connections that vary in males and females is that they are the result of a direct link from the epigenetic ‘landscape’ to the physical landscape of DNA in the organized genomes of species from microbes to man (sans mutations). One of the co-authors of the papers linked above sponsored me for membership in the Society for Neuroscience. I think that he may help me make a point that I’ve been trying to make about epigenetic effects. For comparison, please try to make a point about mutation-initiated natural selection and how it leads to changes in neuronal connections, which now includes the role of specific changes in specific neurons of the human brain.