Scientists uncover striking differences between mouse and human gene expression across a variety of tissues.
November 17, 2014|
Excerpt: “…results published today (November 17) in PNAS reveal widespread differences between human and mouse gene expression, both in protein-coding and noncoding genes, suggesting that understanding these disparities could help explain fundamental differences in the two species’ physiology.”
My comment: See also: Physiology is rocking the foundations of evolutionary biology
Conclusion: “Perhaps the elegant mathematics and the extraordinary reputation of the scientists involved blinded us to what now seems obvious; the organism should never have been relegated to the role of mere carrier of its genes.”
My comment to The Scientist Magazine:
(This model of RNA-mediated cell type differentiation was first presented in our 1996 Hormones and Behavior review.)
The metabolism of nutrients to species-specific pheromones that control the physiology of reproduction in species from microbes to man exemplifies how comparisons of RNA-mediated transcriptional landscapes have since established the validity of Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
“Until recently, the association of the nutrient choline in humans and its metabolism to trimethylamine odor in different species of mice was the best example of how a change in diet becomes associated with the presence of mammalian conspecifics whose androgen estrogen ratio-associated odor distinguishes them sexually, and also as nutrient-dependent physically fit mates (Stensmyr & Maderspacher, 2013). The mouse model makes it clearer that glucose uptake changes cellular thermodynamic equilibrium and differential pathway regulation that results in adaptively evolved fitness in species from microbes (Kondrashov, 2012) to mammals. Species-specific health and reproductive fitness is associated with nutrient-dependent amino acid substitutions and with pheromone-controlled reproduction. Disease is associated with mutations exemplified in cancer where perturbations of the glucose-dependent thermodynamic/thermoregulatory equilibrium are equally clear (Locasale, 2012).
Theorists insist that beneficial mutations somehow lead to increasing organismal complexity manifested in epigenetically altered transcriptional landscapes. Their theories are based on what they learned about conserved molecular mechanisms from population geneticists, which serious scientists now understand is NOTHING AT ALL.
The serious scientists have learned from comparisons of transcriptional landscapes across species and comparisons of morphological AND behavioral phenotypes. See for example, Dobzhansky (1973):
…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla.
Theorists are now forced to claim that amino acid substitutions are akin to mutations. But mutations perturb the chemistry of protein folding, which is why they cannot lead to increasing organismal complexity.
For comparison, amino acid substitutions are linked from the de novo creation of olfactory receptor genes to species diversity in vertebrates and invertebrates via conserved molecular mechanisms of ecological, social, neurogenic, and socio-cognitive niche construction — with examples in my 2013 review.