Automagical disruption of an eQTL (2)

By: James V. Kohl | Published on: July 18, 2017

See: Automagical disruption of an eQTL (1)
The automagical disruption of an eQTL, which linked rs34481144 and influenza could also have been reported in the context of this model.
Nutrient-dependent/pheromone-controlled adaptive evolution: a model
In the model, food energy links the pheromone-controlled physiology of reproduction in all living genera from rs34481144 and other SNPs to species-specific organism-level changes in skin, glands, and hair protection, which link ecological adaptations to protection from the virus-driven degradation of messenger RNA.

Mathematical models vs. biological facts

Random mutations that somehow cause one or more amino acid substitutions are not likely to simultaneously cause adaptive evolution from the bottom up via the thermodynamics of chromatin remodeling and control of adaptive evolution from the top down via organism-level thermoregulation. However the nutrient-dependent substitution of alanine for valine (Grossman et al., 2013; Kamberov et al., 2013) appears to result in species-specific organism-level changes in skin, glands, and hair, through pheromone-controlled reproduction.

See for instance: Modeling Recent Human Evolution in Mice by Expression of a Selected EDAR Variant

An adaptive variant of the human Ectodysplasin receptor, EDARV370A [also known as: rs3827760, 1540T/C, 370A or Val370Ala, is a SNP in the ectodysplasin A receptor EDAR gene on chromosome 2], is one of the strongest candidates of recent positive selection from genome-wide scans. We have modeled EDAR370A [also known as: rs3827760…] in mice and characterized its phenotype and evolutionary origins in humans. Our computational analysis suggests the allele arose in central China approximately 30,000 years ago. Although EDAR370A [also known as: rs3827760…] has been associated with increased scalp hair thickness and changed tooth morphology in humans, its direct biological significance and potential adaptive role remain unclear. We generated a knockin mouse model and find that, as in humans, hair thickness is increased in EDAR370A [also known as: rs3827760…] mice. We identify new biological targets affected by the mutation, including mammary and eccrine glands. Building on these results, we find that EDAR370A [also known as: rs3827760…] is associated with an increased number of active eccrine glands in the Han Chinese. This interdisciplinary approach yields unique insight into the generation of adaptive variation among modern humans.

The adaptive variation links the SNP, rs3827760 to the report on the automagical disruption of the eQTL, which linked rs34481144 to differences in the virulence of influenza in the Han Chinese. Differences in virulence were linked from ecological variation to differences in morphological and behavioral phenotypes via the mouse to human model of energy-dependent pheromone-controlled RNA-mediated cell type differentiation.
The mouse to human model also links the SNP, BDNF Val66Met, from stress-linked damage to DNA to changes in behavior.
Stress dynamically regulates behavior and glutamatergic gene expression in hippocampus by opening a window of epigenetic plasticity reported as: Newly discovered windows of brain plasticity may help with treatment of stress-related disorders
The BDNF val66met polymorphism and individual differences in temperament in 4-month-old infants: A pilot study
The fact that this pilot study is only now starting to link the ATP-dependent creation of RNA from differences in SNPs to differences in morphology and behavior via the pheromone-controlled physiology of reproduction is an embarrassment to all pseudoscientists. They will not admit that they know nothing about RNA-mediated cell type differentiation or how it is prevented by the virus-driven degradation of messenger RNA.

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