Excerpt: “… the discovery that reproductive isolation can be brought about by ecological adaptation in ordinary phenotypic traits bridges Darwin’s science of speciation and our own.
“The most obvious shortcoming of our current understanding of speciation is that the threads connecting genes and selection are still few. We have many cases of ecological selection generating reproductive isolation with little knowledge of the genetic changes that allow it.”
My comment: Experimental evidence of cause and effect supports scientific progress. I used experimental evidence of conserved molecular mechanisms that are obviously responsible for ecological adaptations in the context of nutrient-dependent pheromone-controlled adaptive evolution: a model. I regret the implication that adaptive evolution occurred, but reviews that are not framed in the context of evolution are not well-received. Simply put, researchers must mislead others an make them think their opinions of cause and effect might be validated, or they may not read the latest published works on ecological adaptations, which means the work will not receive critical evaluation.
One critical evaluation of my model was reported in a book in 2011: ‘This model is attractive in that it solves the “binding problem” of sexual attraction. By that I mean the problem of why all the different features of men or women (visual appearance and feel of face, body, and genitals; voice quality, smell; personality and behavior, etc.) attract people as a more or less coherent package representing one sex, rather than as an arbitrary collage of male and female characteristics. If all these characteristics come to be attractive because they were experienced in association with a male- or female-specific pheromone, then they will naturally go together even in the absence of complex genetically coded instructions.” (p. 210)
Since then, experimental evidence to support the model, which solved the “binding problem” of sexual attraction, has continued to accumulate. No experimental evidence supports the idea of mutation-driven evolution of sexual attraction has been published. Instead, Evidence for Mito-Nuclear and Sex-Linked Reproductive Barriers between the Hybrid Italian Sparrow and Its Parent Species portrays ecological adaptations.
Excerpt: “…the fact that HSDL2‘s protein product is located within mitochondria ,  supports its candidacy as an RI gene. HSDL2 is thought to be involved in fatty acid metabolism, although its exact functions are unknown .”
My comment: In my model this fact links the nutrient-dependent protein product to the metabolism of fatty acids to species-specific pheromones that control reproduction. The claim that the exact functions of HSDL2 are unknown are akin to claims that no one knows exactly which fatty acid metabolites might effect the mixture of nutrient-dependent metabolites that act as species-specific pheromone signatures. Despite the model that links nutrient uptake to pheromone production and species diversity, the portrayal of ecological adaptations in this study will probably be critically reviewed as if it exemplified mutation-driven evolution via natural selection for whatever was selected. Only if reviewers dig deep enough into the confusion of the text will they find that one species appears to have been selected for mito-nuclear interactions and loci on the Z chromosome. That links the metabolism of nutrients to species-specific pheromones and chromosomal rearrangements, which places the molecular mechanisms of speciation into the context of biophysical constraints on beneficial mutations. Instead of beneficial mutations, which are not known to occur, nutrient-dependent pheromone-controlled reproduction seems likely to have contributed to de novo gene creation and chromosomal rearrangements that link common molecular mechanisms to species diversity in species from microbes to man.
For comparison, Estrogen receptor α polymorphism in a species with alternative behavioral phenotypes and also with different morphological phenotypes clearly exemplifies nutrient-dependent pheromone-controlled ecological adaptations. The ecological adaptations obviously arise from epigenetic effects of the sensory environment. The adaptations are associated with differences in parental feeding that result in chromosomal rearrangements and in transgenerational epigenetic inheritance of morphological and behavioral phenotypes without reproductive isolation that might lead to speciation.
Everything about the conserved molecular mechanisms that might lead to species diversity goes together in the absence of complex genetically coded instructions in Estrogen receptor α polymorphism in a species with alternative behavioral phenotypes. Nothing that is known about the conserved molecular mechanisms of ecological adaptations fits into the context of Evidence for Mito-Nuclear and Sex-Linked Reproductive Barriers between the Hybrid Italian Sparrow and Its Parent Species. The evidence may initially appear to exemplify mutation-driven evolution, which means a critical evaluation of experimental evidence may already be overdue.
Mutation-driven evolution makes no attempt to solved the “binding problem” of sexual attraction. Thus, the theory does not seem to fit very well into the experimental Evidence for Mito-Nuclear and Sex-Linked Reproductive Barriers. The question arises, how is the physical evidence of nutrient-dependent mito-nuclear interactions linked via mutations to reproductive barriers? The answer to the question can be placed into the context of experimental evidence that links epigenetically-effected Estrogen receptor α polymorphism to alternative morphological and behavioral phenotypes. Experimental evidence that links epigenetically-effected morphology and behavior to species diversity via conserved molecular mechanisms could then be critically reviewed for comparison to explanations of how mutation-driven evolution might somehow result in species diversity.
I suggest that Evidence for Mito-Nuclear and Sex-Linked Reproductive Barriers and Estrogen receptor α polymorphism, which is linked to alternative morphological and behavioral phenotypes, be compared in the context of nutrient-dependent pheromone-controlled de novo creation of olfactory receptor genes. This might lead to an explanation of how mutations appear to result only in the loss of genes accompanied by the creation of pseudogenes. The pseudogenes do not perturb protein folding like mutations do, so the pseudogenes are not eliminated from the DNA of the organized genome like they would be if they were mutated genes that perturbed protein folding. If anything, the pseudogenes appear instead to be placed on hold in case their reactivation and unfolding might be required if the epigenetic effects of food odors and controlled expression of genes by pheromones was ever required for species diversification in an unpredictable environment of ecological variation. There’s a model for that!
Excerpt: The loss of Kiss function in birds may also reflect the plasticity in the neuromediators and their receptors involved in the control of GnRH neurons and reproductive function throughout vertebrate evolution.”
My comment: In my model, stabilization of the genome occurs via the conserved molecular mechanisms of nutrient-dependent pheromone-controlled ecological adaptation and the chromosomal rearrangements that may or may not result in species diversity via substitution of the achiral amino acid glycine in the GnRH peptide that appears to be conserved in the vertebrate genome across 400 million years ecological adaptations. An established biological core of vertebrate reproduction enables rapid diversification of species that fill ecological niches. The ecological niches link differences in the amniote lineage to differences in the sauropsid lineage and the mammalian lineage via nutrient-dependent pheromone-controlled amino acid substitutions that differentiate the cell types of all genera.
The link from olfactory/pheromonal input to nutrient-dependent pheromone-controlled amino acid substitutions and the de novo creation of olfactory receptor genes and to nutrient-dependent pheromone-controlled variations in GnRH pulse frequency establishes the ligand-receptor link between GnRH and its receptor. The ligand-receptor link is the biological basis of my explanations for how the epigenetic landscape becomes the physical landscape of DNA in the organized genomes of species as diverse as egg-laying dinosaurs and birds. Conserved molecular mechanisms of nutrient-dependent pheromone-controlled species-specific reproduction establish how everything known about ecological adaptations in the context of the ecological variations may result in speciation in species from microbes to man.
The alternative to examination of genes and pseudogenes in different lineages is to continue to evoke the idea of “constraint-breaking” mutations in genes that somehow might be responsible for mutation-driven evolution. The biophysical constraints that lead to mammals from amniotes such as dinosaurs and birds can be removed from consideration via suggestion. That suggestion allows some people to continue believing in that mutations led to difference in birds and mammals. Therefore, they can continue to believe that mutation-driven evolution occurs outside the context of biophysical constraints in all genera. However, with beliefs like that, there is no reason to teach students about physics, chemistry, or biology. They need only be taught to believe in Masatoshi Nei’s “constraint-breaking mutations” that he thinks enable Mutation-Driven Evolution.
“…it’s his natural selection-busting theory, which Nei developed in the ’80s and expanded on in the 2013 book Mutation-Driven Evolution, that the researcher wants to see embraced, cited and taught in schools.”
I’m reminded of the song: “Do you believe in magic?” Obviously many people do, but I don’t think that the “magic” of mutation-driven evolution should be taught to students. There’s no model for that. It’s just Nei’s suggestion of what should be taught.