Aerobic glycolysis and amino acid substitutions in the brain (sans mutations)

The complexity of how conserved molecular mechanisms enable ecological adaptations via nutrient-dependent amino acid substitutions that differentiate cell types in individuals of all animal species remains beyond the grasp of evolutionary theorists. Their belief that mutations somehow cause species diversity via natural selection or automagically as recently reconceptualized in the book Mutation-Driven Evolution cannot be addressed unless they stop touting nonsensical theories.

Instead,  earlier today a co-editor of the special issue in which my 2012 review article appeared, tried to draw me into a discussion with this caveat:  “… if he insists that mutations are always deleterious, then that is
clearly false. On rare occasions mutations confer adaptive advantages, and then those genes are more likely to spread through a population.”

Like others, his intent appears to be to discuss with me the ridiculous theory of mutation-driven evolution, when I clearly stated in  Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors that “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans.”

In Nutrient-dependent/pheromone-controlled adaptive evolution: a model, I provided examples of nutrient-dependent pheromone-controlled amino acid substitutions that differentiate cell types and species. I cannot recall anything I’ve written or said that might ever have indicated a role for deleterious or beneficial mutations in ecological adaptations. Thus, there would be no reason for me to insist that “…mutations are always deleterious.”   Instead, even in the book I co-authored in 1995, there was a chapter “From Genes to Behavior and Back” that drew attention to the remarkable role of a single molecule called gonadotropin releasing hormone (GnRH) and it ability to link pheromones to hormones and behavior sans mutations.

Discussion of how the epigenetic landscape becomes the physical landscape of DNA in the organized genome of all vertebrates via olfactory/pheromonal input and GnRH should have long since progressed to include the molecular epigenetics of conserved molecular mechanisms across all species.  However, I realize that this is probably not going to happen in my lifetime. There are too many ignorant theorists to contend with who will not update their knowledge base or consider anything not taught to them by those who never asked about experimental evidence, which might have supported the idea of mutation-driven evolution. There is none, but theorists will argue to their death, or mine, that mutations are not always deleterious and so they must sometimes be beneficial. That is a belief based on ignorance. It is time for a reality check, and the reality check was reported in the context of a Chirality Check.

Excerpt: “Most biological macromolecules are homochiral, and enzymes help to maintain this state of affairs; for example, checkpoints ensure that only l-amino acids are incorporated into proteins during translation.”

My comment: This means the amino acid substitutions that differentiate cell types in individuals of species do not result from uncontrolled intercellular interactions.  It means that the controlling factor is chirality which ensures functional protein folding by matching molecules of d-glucose and l-amino acids that result in amino acid substitutions. These amino acid substitutions do not perturb the protein folding that must occur for cells to maintain their functions. Those functions vary with the receptor-mediated diversity of cell types.

What role do mutations play in this diversity? None! Mutations perturb protein folding. This may not be of concern if the damage to cell function is minimal, but no mutation-initiated damage is ever going to somehow enable an organism’s ecological adaptation.  If theorists could move beyond that nonsense, they might someday arrive at factual representations of cause and effect like this:

Mechanism of chiral proofreading during translation of the genetic code

Excerpt (with my emphasis): The conserved and indispensable nature of the motif in DTD argues strongly for its crucial role in solving this key chiral discrimination problem in biology. The presence of DTD-fold and function in all kingdoms of life suggests an important role such systems have played in enforcing homochirality during early evolution of the translational apparatus, and high levels of expression in neuronal cells indicate a crucial role of DTD in higher organisms, which still needs to be explored.

My comment: The substitution of achiral glycine in the GnRH molecule of vertebrates stabilizes nutrient-dependent pheromone-controlled protein folding in the cells of tissues in all vertebrates. That means it links glucose uptake to aerobic glycolysis and amino acid substitutions in the cell types of human brain tissue to the experience-dependent mosaicism of glucose-facilitated ecological adaptations with no consideration for whatever any theorists thinks might be attributed to beneficial mutations if ever there is experimental evidence to support their existence. It is the Mosaic Copy Number Variation in Human Neurons that links our brain development to brain development in invertebrates and to the continuum of nutrient-dependent pheromone-controlled ecological adaptations in species from microbes to man via amino acid substitutions.

One straightforward hypothesis is that neurons with different genomes will have distinct molecular phenotypes because of altered transcriptional or epigenetic landscapes.

Support for that hypothesis can be found in everything I have ever published, and everything published by people like Ryzsard Maleszka and other researchers whose focus is the honeybee model organism. See for example: DNA methylation dynamics, metabolic fluxes, gene splicing, and alternative phenotypes in honey bees and Epigenomics and the concept of degeneracy in biological systems. Meanwhile, I’m becoming ever more suspicious of people who want me to comment about the role of  mutations, which they seem to think confer adaptive advantages, when I have already clearly stated repeatedly that there is no such thing as an adaptive mutation. There are too many people who already have twisted what I’ve fully-detailed and made it seem like it was something other than the biological facts of how ecological adaptations occur. Thus, as others come closer to realizing the difference between mutation-driven evolution and ecological adaptations, I expect that many of them will attempt to make it appear that they knew all along about the importance of nutrient-dependent pheromone-controlled adaptations.

Author: James Kohl

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