Epistasis: the epigenetics of emergent phenotypes (revisited)

By: James V. Kohl | Published on: November 8, 2013

Follow-up to The epigenetics of emergent phenotypes  March 25, 2013
I flagged a few symposium abstracts from the Society for Molecular Biology and Evolution for follow-up, and was waiting to thoroughly address the issue of transposable elements in the context of mutation-driven evolution in moths and butterflies. Now I see that other presenters are the first to challenge — with experimental data — all aspects of mutation-initiated natural selection in all species. Their genius shows in the way they present that challenge. However, I think their publication in “Nature” puts them in an awkward position. Others will probably recognize the importance of their work to a paradigm shift that dispenses with the theory of natural selection via predation by birds in moths and natural selection in the development of the human brain via snake predation in primates. Evolutionary theorists are not likely to enjoy being faced with evidence that Genetic incompatibilities are widespread within species. They will lose forever their ability to tout random mutations as an explanation of anything but diseases and disorders.
Article excerpt: “…the raw material to drive reproductive isolation is segregating contemporaneously within species and does not necessarily require… the emergence of genetically incompatible mutations independently derived and fixed…”
My comment: No experimental evidence suggests that mutations are fixed in the DNA of the organized genome of any species from microbes to man. Now, experimental evidence from Drosophila adds another model organism to experimental evidence from the model organism C. elegans. Mutations are not fixed in either model organism.
At at time when theoretical biologists are extracting physics from biophysics in an effort to remove natural selection from mutation-initiated natural selection, what we have is probably a permanent replacement of the Dobzhansky–Muller incompatibility (DMI) model of theoretical biology (sans physics) with an accurate representation of  genotype ratio distortion (GRD) and the biophysics involved in epistasis.
In Kohl (2013) I wrote: “Current concepts now limit attempts to explain selection for nutrient-dependent changes in coat color and kinked tails in mice via mutations theory, since mutations theory does not address pleiotropy and epistasis (see for review Feinberg & Irizarry, 2010).” Those authors suggested that epigenetically-effected natural selection in social insects that show environment-mediated phenotypic differences in social castes might make the honeybee model organism a great model for testing such ideas, which is one reason I used the honeybee model organism in my model (see Kohl, 2012).
Then, in Kohl (2013) I concluded that “Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.”
The DMI model of theoretical biology does not fit. The GRD model appears to fit perfectly into the context of nutrient-dependent pheromone-controlled adaptive evolution.
 


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