Nutrient-dependent RNA-mediated cause and effect

Could the food we eat affect our genes? Study in yeast suggests this may be the case


Excerpt: “Cellular metabolism plays a far more dynamic role in the cells than we previously thought,” explains Dr Ralser. “Nearly all of a cell’s genes are influenced by changes to the nutrients they have access to. In fact, in many cases the effects were so strong, that changing a cell’s metabolic profile could make some of its genes behave in a completely different manner.
“The classical view is that genes control how nutrients are broken down into important molecules, but we’ve shown that the opposite is true, too: how the nutrients break down affects how our genes behave.”

My comment: Nutrient-dependent metabolic networks are linked to genetic networks. The epigenetic effect of nutrients is linked to hormones that affect the behavior of all vertebrates and invertebrates via conserved molecular mechanisms that link microbes to humans.

From Fertilization to Adult Sexual Behavior



In this regard it seems important to emphasize that chemosensory communication is ubiquitous throughout life among species from single celled yeasts to primates, including humans (see for review Kohl and Francoeur, 1995). Chemical stimuli, odors, including pheromones, are essential components of reproductive sexual behavior in most, if not all, species. Pheromonal communication has been seen to elicit physiological and behavioral changes that benefit both male and female individuals and, in humans, these olfactory sensations seem to exert their influence whether or not an individual is conscious of odor detection.
Evolutionary conservation, both of pheromonal communication and its importance to behavior, is indicated by the involvement of a key mammalian reproductive hormone. For instance, a yeast pheromone, the alpha-mating factor, is very similar in structure to mammalian gonadotropic releasing hormone (GnRH). When injected into rats, this chemical binds to pituitary GnRH receptors and brings about the release of LH. Loumaye, Thorner, and Catt (1982) note: “GnRH and the yeast alpha-mating factor appear to represent a highly conserved effector system which includes the peptide ligand, the cell-surface receptor, and the physiological regulation of reproductive function” (p. 1325).

See also:
Non‐enzymatic glycolysis and pentose phosphate pathway‐like reactions in a plausible Archean ocean
Regulation of ribosomal DNA amplification by the TOR pathway
Conditional iron and pH-dependent activity of a non-enzymatic glycolysis and pentose phosphate pathway
Other Publications from Ralser (Ralser’s group 2005- 2015)
My comment: It has been 20 years since we linked what organisms eat and the pheromones they produce to chemosensory communication throughout life among species from single celled yeasts to primates via a highly conserved RNA-mediated effector system which includes the peptide ligand, the cell-surface receptor, and the physiological regulation of reproductive function.
It has been 10 years since Nobel Laureate, Linda Buck co-authored Feedback loops link odor and pheromone signaling with reproduction (2005)
Obviously, something has gone horribly wrong. The metabolic background is a global player in Saccharomyces gene expression epistasis was published and reported in the context of a question. Could the food we eat affect our genes?
Everything known to serious scientists about biophysically constrained RNA-mediated protein folding chemistry and cell type differentiation links nutrient-dependent amino acid substitutions to the stability of supercoiled DNA in the organized genomes of all living genera.  How could anyone not know that the supercoiled DNA links metabolic networks and genetic networks to epistasis. Why would anyone ask “Could the food we eat affect our genes?” Why would anyone suddenly claim that a “Study in yeast suggests this may be the case.”
What experimental evidence of biologically-based cause and effect suggested that a case could be made for any other links from atoms to ecosystems?

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