Eliminating selfish genes and accidental species

The Selfish Gene is losing friends

Is the ‘inclusive fitness’ model that underpins evolutionary science flawed?

Excerpt: “Whatever the final verdict, this dispute will become a case study for historians interested in how much mathematical rigour – of the kind that gave us Newton’s laws and more besides in physics – can be tolerated by messy, complex, wet biology. After this reckoning, we may better understand the difference between mob rule and academic consensus, and how to distinguish “pathological science” driven by wishful thinking from the creative insights of true scientific visionaries.”

The Accidental Species by Henry Gee, review

New books shed light on the ascent of man, but many mysteries remain, says Caspar Henderson

Excerpt: “Denisovans, only identified in 2010, mated not only with both our ancestors and Neanderthals but (scientists determined just this year) another mysterious population of archaic humans that lived in Asia more than 30,000 years ago that was neither modern human nor Neanderthal.
My comment: Harvard researchers reported in January (2013) that a population of modern humans arose in what is now central China during the past ~30,000 years due to an amino acid substitution in a receptor, which was attributed to a change in a single base pair.
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In Kohl (2013), I wrote: “Two additional recent reports link substitution of the amino acid alanine for the amino acid valine (Grossman et al., 2013) to nutrient-dependent pheromone-controlled adaptive evolution. The alanine substitution for valine does not appear to be under any selection pressure in mice. The cause-and-effect relationship was established in mice by comparing the effects of the alanine, which is under selection pressure in humans, via its substitution for valine in mice (Kamberov et al., 2013).
These two reports (Grossman et al., 2013; Kamberov et al., 2013) tell a new short story of adaptive evolution. The story begins with what was probably a nutrient-dependent variant allele that arose in central China approximately 30,000 years ago. The effect of the allele is adaptive and it is manifested in the context of an effect on sweat, skin, hair, and teeth. In other mammals, like the mouse, the effect on sweat, skin, hair, and teeth is due to an epigenetic effect of nutrients on hormones responsible for the tweaking of immense gene networks that metabolize nutrients to pheromones. The pheromones control the nutrient-dependent hormone-dependent organization and activation of reproductive sexual behavior in mammals such as mice and humans, but also in invertebrates as previously indicated. That means the adaptive evolution of the human population, which is detailed in these two reports, is also likely to be nutrient-dependent and pheromone-controlled, since there is no other model for that.”
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Earlier this week, we learned that amino acid substitutions in olfactory receptor genes distinguish species-specific individuality of human olfactory receptor neurons. These neurons are linked to the perception of odors and thus to differences in behavior in roundworms, invertebrates, and vertebrates. The report on the amino acid substitutions said:  ” …these data provide a solid platform from which to probe the effects of a single odorant receptor on olfactory perception.”
If the experience-dependent nutrient-dependent changes in base pairs and single amino acid substitutions in other species are used to probe how species-wide ecological adaptations occur, there will be no more need for mathematical models of fitness and no more need for evolutionary theory. Researchers can begin to approach the obvious relevance of species diversity to human disease in the context of biological facts and conserved molecular mechanisms. Academic consensus will forever be recognized as “pathological science” driven by wishful thinking. However, this will not prevent those who Dobzhansky inferred were useless bird-watchers and butterfly collectors from continuing their attempts to suppress creative insights. Dobzhansky (1964) wrote: “The notion has gained some currency that the only worthwhile biology is molecular biology. All else is “bird watching” or “butterfly collecting.” Bird watching and butterfly collecting are occupations manifestly unworthy of serious scientists!
Teresa Binstock (1996) wrote: “Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation…” We have since learned that these alternative splicings link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man via amino acid substitutions. What we’ve learned about conserved molecular mechanisms has continued to be suppressed by evolutionary theorists. But the best that will happen now, is that as science progresses more of the people who have been responsible for academic suppression of creative insights will be recognized and removed from their positions. When that happens, the paradigm shift that Dobzhansky (1964) and Binstock (1996) predicted will continues to propel us forward.

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