Pre-existing genetic variability or random mutations: a matter of priorities and choices
April 25, 2012 | James Kohl
“The study, published online today in Nature, shows that bacteria have evolved a mechanism
that protects important genes from random mutation, effectively reducing the risk of self-destruction.”
My comments on what the actual article tells us in: Evidence of non-random mutation rates suggests an evolutionary risk management strategy
Non-random mutation, as evidenced by ‘hot’ and ‘cold’ genes involved in amino-acid biosynthesis, energy metabolism, and catabolism of specific compounds is compatible with a model where 1) nutrient chemicals calibrate intracellular signaling and stochastic gene expression, and 2) the metabolism of nutrients to pheromones standardizes and controls reproduction.
This is the model detailed in Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. The honeybee is the invertebrate model organism that extends the common molecular biology across species from microbes to man, but additional support for my conceptualization can now be found in what was recently reported on threespine stickleback fish, a vertebrate model organism of speciation.
Evolutionary theorists have been loudly shouting for years that “[RANDOM] Mutations are the reason each of us is unique. These changes to our genetic material are at the root of variation between individuals, and between cells within individuals.” Indeed, it seems that the theorists may continue to focus on non-random mutations instead of the more obvious scientifically established fact that pre-existing genetic variation enables adaptive evolution, and random mutation does not.
For example, the pre-existing genetic variation that allows a cell to adapt to changes in the availability of nutrients from its environment appears to have be programmed into the first living cell(s). Receptor-mediated cellular changes in metabolism of the nutrients enable cell to cell signaling that varies with the metabolism of nutrients to pheromones.
This fact can be explained to a general audience by saying that food odors cause us to eat what causes us to produce pheromones that cause us to associate, or not associate, with other people. In this context, pheromones are social odors.
A matter of choices:
Pre-existing genetic variations across species makes food choice essential to individual survival, and it makes mate choice essential to species survival in species that sexually reproduce. An organism that eats the wrong food may not live to reproduce. Clearly, the pre-existing genetic variations make the effects of different foods on hormones that affect our behavior a key indicator of how pre-existing genetic variability can effect hormones and their metabolism to pheromones that cause changes in sexual behavior.
The allegorical representation of this newly established scientific truth occurs in Genesis with a story indicating that what Eve decided to eat epigenetically altered events across Creation (i.e., based on pre-existing genetic variability, not random mutations). Nevertheless, incorporating similar important choices into thoughts and decisions about what we eat and our mate choice may be easier for those who continue to think the development of their behavior was determined by random mutations. After all, who’s going to hold them accountable for not recognizing the truth about the difference between pre-existing genetic variations and random mutations?