Excerpt: Overall, our results underscore the importance of comparing divergent model organisms to human to highlight conserved biological principles (and disentangle them from lineage-specific adaptations).
My comment: In the detailed comparisons of divergent model organisms portrayed in Nutrient-dependent/pheromone-controlled adaptive evolution: a model, I underscored what is known about cell type differentiation in species from microbes to man. By placing what is known into the context of nutrient-dependent amino acid substitutions and biodiversity controlled by the metabolism of nutrients to species-specific pheromones, I thought it would be clear that the best approach to understanding how biodiversity arose was to model it. Conclusion: “Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.”
The model arose from prior published works that clearly linked the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man. See for example: Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Conclusion: “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans…”
Now “…comparing divergent model organisms to human…” continues “…to highlight conserved biological principles…”
These conserved biological principles are obviously the conserved molecular mechanisms of nutrient-dependent pheromone-controlled cell type differentiation we detailed in our 1996 Hormones and Behavior review article in the context of sex differences in cell types. Did anyone who is not an evolutionary theorist think that cell type differentiation occurred differently in different cells of different individuals in different species?
See for review our section on: “Molecular epigenetics” in From Fertilization to Adult Sexual Behavior
“Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.”
See also: Alternative RNA Splicing in Evolution but try to think in terms of how ecological variation leads to ecological adaptations via nutrient-dependent alternative splicing of pre-mRNA. I tried to convey this message yesterday: There are no evolutionary events. There are only epigenetically-effected amino acid substitutions that differentiate cell types and pheromone-controlled cell type differentiation enables biodiversity. There is no model of how biodiversity arises via evolutionary events, because it doesn’t.