Deletions, duplications, and other mutations
November 1, 2013 | James Kohl
Excerpt: “…Darwin’s theory of evolution ultimately abetted a modern conceit—that the genomes in our cells are highly optimized end products of evolution.”
My comment: The ability to adapt to changes in the epigenetic ‘landscape’ is nutrient-dependent and pheromone-controlled in species from microbes to man.
Excerpt: “Deletions, duplications, and other mutations may arise at different places in a developmental lineage.”
My comment: This perspective starts with the false premise that duplications (e.g., copy number variants) are mutations as if that misrepresentation was part of Darwin’s theory. Darwin knew nothing about genetics or epigenetics. Darwin’s theory did not cast duplications in the light of deletions or other mutations. Instead, Darwin repeatedly stated that ‘conditions of life’ were of primary concern before any consideration could be give to natural selection (e.g., for deletions or mutations).
Conditions of life are nutrient-dependent and so are copy number variants in yeasts (unicellular organisms). In yeasts, nutrient-dependent pheromone-controlled reproduction is the mechanism through which one signaling pathway involved in nutrient uptake regulates a second pathway for pheromone-controlled reproduction. The regulation of pheromone production by nutrient uptake is how cells integrate different signals that enable them to produce a coordinated response. The coordinated response ensures that the organized genomes of all cells in all extant organisms are the highly optimized end products of evolution.
In neurons of the human brain, copy number variants are determined by nutrient uptake and reproduction is controlled by pheromones. This means that neuronal copy number variants are controlled by nutrient-dependent production of pheromones via conserved molecular mechanisms of microbes to man. Attempting to portray copy number variants as duplications that are like other mutations skews any other proper perspective that might have been provided by these authors.
It is simply not possible to start with a false premise, attribute it to Darwin, and then move forward to any sensible explanation of biologically based cause and effect. Instead, let’s start with the fact that: ‘One of the main duplicated gene families are the olfactory receptor proteins [18,117–119] so perhaps their duplication may lead to an increase in sensitivity to a particular odour may be adaptive under certain conditions.“That means the experience-dependent de novo creation of olfactory receptor genes and their duplication is controlled by the metabolism of nutrients to species-specific pheromone blends that control reproduction. That fact makes sense of why there are copy number variants in neurons of the human brain and in unicellular yeasts. The molecular mechanisms that enable nutrient-dependent pheromone-controlled copy number variants are the same are the same.