Beneficial epistatic mutations?

Re: Covert, Lenski, Wilke and Ofria (2013) Experiments on the role of deleterious mutations as stepping stones in adaptive evolution. PNAS doi: 10.1073/pnas.1313424110

What’s in a (mutation’s) name?

Excerpt: “Every once in a while, a deleterious mutation will interact with other mutations in a way that makes them more beneficial together; interactions such as these are known in the literature as “epistatic” mutations.”

My comment: The idea of epistatic mutations is fascinating. Thanks, but in “Multiple Overlapping Genetic Codes Profoundly Reduce the Probability of Beneficial Mutation” the idea of mutation-driven evolution is thoroughly trashed. That’s why I was surprised to find your report on your work linked by Danielle Whittaker who recently reported with others that birds sniff out their mates.

That accurate representation of mate choice in birds is based on the concept of nutrient-dependent pheromone-controlled epistasis and adaptive evolution in species from microbes to man. It makes me wonder if there is a way to extend your statistics to what is known about the physiology of reproduction and thereby link two “epistatic” mutations to beneficial thermodynamics involved in stochastic gene expression or to organism-level thermoregulation as is required for adaptive evolution sans mutations theory.

I’m thinking more in terms of Darwin’s ‘conditions of life’ as opposed to probability theory, since we know his ‘conditions of life’ are nutrient-dependent and pheromone-controlled (sans mutations) even in birds. When I see that pattern across species, I wonder if pattern recognition might be incorporated into your thoughts about how epistatic mutations might be involved in ecological, social, neurogenic, and socio-cognitive niche construction, which seems to have been a requirement for our adaptive evolution. For example, in Kohl (2013) I wrote:

“The mouse odor also repels humans. High excretion rates of trimethylamine-associated odor in humans cause ‘fish odor syndrome’. The aversive body odor has been attributed to a mutation (Dolphin, Janmohamed, Smith, Shephard, & Phillips, 1997). This attribution is not consistent with the portrayal of synergy in the mouse model, which enables both the production of the odor and the response to the odor.

This synergy requires at least two things to happen simultaneously: for example, (1) natural selection for nutrient chemicals and (2) sexual selection for odor production. Sexual selection for nutrient-dependent odor production is not likely to be achieved via one mutation involved in nutrient acquisition and another mutation that is involved in odor production because two mutations are not likely to simultaneously occur.”

When statistical analyses report what does not seem to be an accurate representation of cause and effect, or when inconsistent reports appear within months of each other, I always ask myself: Is there a biologically based model for that? I quit asking if there was a statistical model for such things because they are much more commonly found.