microRNAs (miRNAs) and adaptive evolution
Theoretically, you may make mutations responsible for diversified life, although biological facts tell us life is nutrient-dependent. When life is nutrient-dependent and diversification of life is due to mutations, there are no known controls on mutation-driven adaptive evolution. When life is nutrient-dependent and controlled by the metabolism of nutrients to pheromones that control reproduction in species from microbes to man, nutrient-dependent species-specific pheromone production controls the diversification of life. For example:
In my model this allows use of the nutrient-dependent pheromone-controlled microRNA/messenger RNA balance to detail adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction (e.g., because the molecular mechanisms are common among species from microbes to man).
Until now, I have preferred to exemplify nutrient-dependent pheromone-controlled adaptive evolution with the honeybee model organism. I think it best represents what happens in eusocial organisms. Others may prefer to look at the latest data from Drosophila and use flies to exemplify nutrient-dependent pheromone-controlled adaptive evolution. I don’t have a problem with the animal model that’s used because I agree with Stephen M. Cohen, who wrote: “At the cellular level much is similar between flies and mammals. This allows the possibility of using fly models for discovery of biological mechanisms relevant to all animals.” I just hope that others don’t have a problem learning that adaptive evolution is not driven by mutations.
Adaptive evolution is 1) nutrient-dependent and 2) pheromone-controlled as indicated in the links I just provided.
The similarities between how the microRNA/messenger RNA balance regulates nutrient-dependent pheromone-controlled reproduction in male flies (above) and how the microRNA/messenger RNA balance regulates reproduction in female mammals will become clearer when MiR-200b and miR-429 Function in Mouse Ovulation and Are Essential for Female Fertility moves from restricted early release in Science Express to publication in Science. The added clarity is predictable by focus on luteinizing hormone (LH) in the abstract.
miR-200b and miR-429 are required to regulate the female hypothalamic pituitary gonadal (HPG) axis via gonadotropin releasing hormone (GnRH)-modulated changes in LH that support ovulation/fertility, steroidogenesis, brain development, and pheromone production. In the 2012 rendition of my model, the epigenetic effects of food odors and of pheromones on mammalian GnRH, LH, ovulation/fertility, steroidogenesis, brain development, pheromone production and properly timed adaptively evolved reproductive sexual behavior are clear. To a lesser degree, so is the fact that every aspect of the complex systems biology of mammalian female fertility and behavior is regulated by exquisitely fine tuned changes in the microRNA/messenger RNA balance. That’s why I’ve added information on the importance of the microRNA/messenger RNA balance to the 2013 rendition of my model. Additional information about the microRNA/messenger RNA balance can be found here.
I felt the additional information should be published as a separate article due to the added complexity of the thermodynamics and organism-level thermoregulation. However, I have not been in a hurry to publish because my antagonists have not yet taken the time to read any of my published works, and they will not be ready to move forward until they do read them.
Clearly, people are not going to understand the importance of molecular epigenetics and alternative splicings (see for example: From Fertilization to Adult Sexual Behavior) to adaptive evolution until they divorce their opinions about evolution from their ridiculous theories. At that point, however, by examining biological facts, they can move forward to learn that the alternative splicings are altered by the microRNA/messenger RNA balance, which is nutrient-dependent and pheromone controlled as exemplified in the mouse model of female fertility and the male fly model of sexual differentiation of the brain, pheromone production, and sexual behavior.
