Molecular time travel: a misrepresentation of amino acid substitutions

Evolution depends on rare chance events, ‘molecular time travel’ experiments show

Excerpt: Thornton and Harms then created millions of copies of this genetic template, using a method that introduced random mutations into every new copy, thus mimicking the variation that evolution could have produced in the protein under alternative scenarios.

My comment: Natural genetic engineering enables the de novo creation of olfactory receptor genes that enable nutrients to alter the microRNA/messenger RNA balance, which leads to amino acid substitutions that differentiate cell types and stabilize the genome when functional receptors are produced. Looking too far downstream — at receptors produced later than those that allow nutrients to enter the cell — reveals the fact that researchers often may report (or think) they are creating something (e.g., millions of copies that introduce random mutations) when the de novo creation of all receptors in all cell types is nutrient-dependent and controlled by the metabolism of nutrients to species-specific pheromones. Pheromones control the physiology of reproduction and thus they control nutrient-dependent ecological speciation when organism-level thermoregulation results from seemingly futile thermodynamic cycles of protein biosynthesis and degradation.

As researchers begin to understand how receptor-mediated behaviors are controlled by nutrient-uptake and pheromones, we should begin to read less On evolutionary causes and evolutionary processes. However, we should already have learned more about biophysically-constrained cell-type differentiation from researchers — primarily in Israel — who continue to report on the conserved molecular mechanisms that enable ecological variation to result in ecological adaptations, which are manifested in morphological and behavioral phenotypes in species from microbes to man.

See, for example: Gene duplication as a mechanism of genomic adaptation to a changing environment “One of the main duplicated gene families are the olfactory receptor proteins [18,117–119] so perhaps their duplication may lead to an increase in sensitivity to a particular odour may be adaptive under certain conditions.” Some would argue that this is not the case for humans — as if the molecular epigenetics of our behavior somehow “evolved” differently. However, there is no model for that, and no experimental evidence suggests anything except conserved molecular mechanisms.

In my model, “… it is interesting to note that the presence of the X-linked Kalig 1 gene affects olfaction, GnRH, LH, androgen/estrogen ratios, and sexual behavior as a result of Kal protein deficiency.  Afflicted patients are genetically predisposed by a single gene to be both anosmic and hypogonadal.  In a small cohort, their sexual behavior is not unlike that of anosmic mammals of other species that lack sexual motivation.  However, Bobrow, Money, and Lewis (1971) have also indicated that these individuals even lack the uniquely species-specific human experience of falling in love.  It is possible, therefore, that a single gene might have dramatic effects on the development of human odor-associated sexual preferences.” (Kohl, 2007)

See also: Evolution of minimal specificity and promiscuity in steroid hormone receptors. “We show that [ the steroid hormone receptors] SRs evolved according to a principle of minimal specificity: at each point in time, these proteins evolved to be specific enough to distinguish among the substances to which they were naturally exposed, but not more so.” Harms and Thornton, with others, have commented on how unlikely it would be if the minimal atomic-level specificity required to link the epigenetic landscape to the physical landscape of DNA in organized genomes was mutation-driven.

“…replacements subtly changed the chemistry of two amino acids, but they dramatically reduced estrogen sensitivity by introducing an excess of interaction partners into the receptor/estrogen complex, inducing a frustrated ensemble of suboptimal hydrogen bond networks unique to estrogens.”

Suboptimal protein folding (i.e., mutation) seems unlikely to lead from nutrient uptake to controlled reproduction that involves amino acid substitutions and the creation of estrogen receptors. For example, Estrogen receptor α polymorphism in a species with alternative behavioral phenotypes makes it clearer that Harms and Thornton (2014) are reporting their findings in terms of mutations, natural selection, and evolution because most people have been taught to believe in that pseudoscientific nonsense, and have ignored the biological facts that link ecological variation to ecological adaptations via amino acid substitutions.

Author: James Kohl

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