learning and memory in unicellular yeasts is exemplified via epigenetically-effected changes in
gonadotropin releasing hormone (GnRH) secretion in young mammals
The authors are among many, who seem to have missed a likely epigenetic link from maternal and/or acquired ferritin deficiency to thyroxine transport, brain development, and behavior.
A single note accurately represents what is known about the epigenetic effects of nutrient chemical-dependent (i.e., glucose-regulated) survival, growth, and the advent of sexual reproduction in microbes like yeasts. It extends my model from microbes to man via the common molecular mechanisms
a molecule similar to GnRH is essential to nutrient chemical-dependent and pheromone-controlled reproduction in all species, including C. elegans.
Patisaul et al (2012) makes it clearer the “The role of oxytocin, for example, must be explained in the context of how pheromones, food odors, and endocrine disruptors epigenetically effect sociosexual behavior.”
Kudos to them for moving us forward and away from random mutations theory to an era where geneticists and neuroscientists can examine sensory cause and effect in the proper perspective of an epigenetic continuum of unconscious affects on genomic interactions…
The epigenetic effects are on interactions among all the other neuronal systems and hormone secretion that interact with the GnRH neuronal system, which is central to all developmental differences in the brain of males and females.
…yeast cells managed to evolve into intelligent mammals, which means there is still hope that your co-workers might do so through the epigenetic effects of nutrient chemicals and pheromones.