Mutation-driven evolution versus the physiology of reproduction

September 10, 2013 | James Kohl

  • Not Exactly Rocket Science (National Geographic):

Mercenary Ants Protect Farmers With Chemical Weapons by Ed Yong

Excerpt: “…they very astutely compare the mercenary ants to a human disease called sickle cell anaemia. It’s an inherited genetic disease that warps the shape of red blood cells and causes a gradual building illness.”

My comments (excerpted from my series of comments on the National Geographic site):

1) Comparing genetically predisposed nutrient-dependent pheromone-controlled behavioral development in insects to a mutation-caused disease in humans stretches the imagination far beyond any model of genetic or of epigenetic cause and effect….

2) Perhaps the metaphor (e.g., something akin to the selfish gene metaphor) should be left to prevail. But that’s not where scientific pursuits are headed. Indeed, many of today’s scientists have actually begun to look for explanatory power in their opinions about cause and effect. They’ve learned that mutation-driven evolution explains nothing.

3) My objection [to “mutation driven” explanations]  is based on the fact that the only way the epigenetic landscape clearly becomes the physical landscape of DNA in any organized genome is via de novo creation of olfactory receptor genes. Creation enables all other receptor-mediated interactions, which are required to epigenetically link the sensory environment to genes and behavior and back. Nutrient-uptake is the bottom-up approach to that link: behavior (at the cellular level) is required for nutrient uptake. That nutrient-dependent “behavior” is controlled from the top-down by the metabolism of nutrients to species-specific pheromones that control reproduction.

Mutation-driven evolution simply does not enter any explanation of cause and effect in the context of the physiology of reproduction, and yet mutations theory continues to show up in metaphors and in misrepresentations of randomly-driven adaptations to predation…

I’ve often wondered if people who tout things like that are familiar with the fact that the pattern of migration in the peppered moth example of industrial melanism was 2 km/night, which precisely matches the distance some male moths will fly to find the female who is producing nutrient-dependent pheromonal signals of reproductive fitness that control reproduction in species from microbes to man. Whenever I ask about that, however, people seem too embarrassed to consider anything else but theory, which is akin to an unending series of books titled “evolution for dummies.”

Simply put, my objection to “mutation driven” explanations is that they explain nothing about adaptive evolution, since they do not address the physiology of reproduction.

I noticed the mention recently, however, of “epistatic mutations” that obviously must somewhat simultaneously occur. This indicates to me that virtually no scientific progress has been made since the statistical bastardization of Darwin’s theory. Now, instead of mutation-driven evolution, we have “mutation(s)-driven” evolution, where one deleterious mutation leads to another mutation and the combination results in a beneficial mutation.

In the context of sickle cell [and the metaphor in Ed Yong’s article], for example see: “Epistasis Among Adaptive Mutations in Deer Mouse Hemoglobin” [subscription required] and my comment on the article [inserted below].

In my model species-specific epistasis is nutrient-dependent and pheromone-controlled. An additional example of this showed up earlier this week in the context of the epigenetically-effected microRNA/messenger RNA balance: “miR-124 controls male reproductive success in Drosophila

miR-14 acts in neurosecretory cells in the adult brain to control metabolism and miR-124 acts in the context of brain-directed neuroendocrine control of sexual differentiation and male pheromone production, which is controlled in mammals by gonadotropin-releasing hormone (GnRH) neurosecretory cells of the hypothalamus.

We can anticipate extension to mammals of the Drosophila model from the abstract of a forthcoming Science article: “MiR-200b and miR-429 Function in Mouse Ovulation and Are Essential for Female Fertility.” Given our earlier work in the context of molecular epigenetics and the concept of alternative splicings and sexual differentiation in Drosophila and C. elegans, I suspect we will see evidence for nutrient-dependent  adaptive evolution of GnRH pulse frequency-controlled LH secretion and pheromone-controlled female fertility in mice.

If I’m correct, this evidence will link glucose and pheromones to feedback loops that control reproduction in invertebrates and vertebrates. (See Nutrient–dependent / pheromone–controlled adaptive evolution: a model). Model organisms exemplify these feedback loops in microbes, nematodes, insects, and other mammals. The mouse to human example that Kamberov et al., and Grossman et al., detailed is the most telling.

A single amino acid substitution appears to result in what seem to be nutrient-dependent changes in the thermodynamics of intracellular signaling, intranuclear interactions, stochastic gene expression, and selection for phenotype via organism-level thermoregulation in a human population that arose in what is now central China during the past ~30K years.

Using a model that integrates what is known about the common molecular mechanisms may help establish whether adaptive mutations lead to thermodynamic effects on organism-level thermoregulation and epistasis, or whether epigenetic effects of nutrients and their metabolism to species-specific pheromones that control reproduction via changes in the microRNA/messenger RNA balance are the driving force behind adaptive evolution in species from microbes to man.

ADDENDUM: It’s “not  exactly rocket science”  to suggest epigenetic effects of nutrients and their metabolism to species-specific pheromones that control reproduction via changes in the microRNA/messenger RNA balance are the driving force behind adaptive evolution in species from microbes to man. The suggestion is made based on everything that is currently neuroscientifically known. Neuroscience is not rocket science, but it’s certainly not akin to the nonsense of evolutionary theory, which lacks any scientific substantiation whatsoever.

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James Vaughn Kohl

James Vaughn Kohl

James Vaughn Kohl was the first to accurately conceptualize human pheromones, and began presenting his findings to the scientific community in 1992. He continues to present to, and publish for, diverse scientific and lay audiences, while constantly monitoring the scientific presses for new information that is relevant to the development of his initial and ongoing conceptualization of human pheromones.