Social learning depends on pheromones.
Science 26 April 2013:
Vol. 340 no. 6131 pp. 483-485
Potent Social Learning and Conformity Shape a Wild Primate’s Foraging Decisions [subscription required]
Abstract Excerpt: “…powerful effects of social learning represent a more potent force than hitherto recognized in shaping group differences among wild animals.”
Social influences on nutrient acquisition involve the same molecular mechanisms of reciprocity all across species. For example, among different bacterial species existing in similar environments, DNA uptake appears to have epigenetically ‘fed’ interspecies methylation and speciation via conjugation. This indicates that reproduction began with an active nutrient
uptake mechanism in heterospecifics and that the mechanism evolved to become symbiogenesis in the conspecifics of asexual organisms. In yeasts, epigenetic changes driven by nutrition might then have led to the creation of novel cell types, which are required at evolutionary advent of sexual reproduction.
These epigenetic changes probably occur across the evolutionary continuum that includes both nutrition-dependent reproduction in unicellular organisms and sexual reproduction in mammals. For example, ingested plant microRNAs influence gene expression across kingdoms. In mammals, this epigenetically links what mammals eat to changes in gene expression and to new genes required for the evolutionary development of the mammalian placenta and the
human brain.
van de Waal, Borgeaud and Whiten provide a primate study that fast-forwards what is known about the evolution of mammals from microbes and invertebrates. Their work exemplifies nutrient-dependent pheromone-controlled adaptive evolution, which occurs via ecological, social, neurogenic, and socio-cognitive niche construction.
Note, however, that the primate socio-cognitive niche arises as does the nutrient-dependent pheromone-controlled socio-cognitive niche of the honeybee model organism. What the queen eats determines her pheromone production, which epigenetically effects every interaction in the colony.”
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I hope this comment to Science will make it more difficult for any intellectual property thief to claim their understanding of the role of microRNAs does not follow from my details of the role of the microRNA / messenger RNA balance in nutrient-dependent pheromone-controlled adaptive evolution. Other researchers may already understand nutrient-dependent pheromone-controlled adaptive evolution in the context of the microRNA / messenger RNA balance. However, as discussion-group participants know, there are always those who are extremely critical of new concepts, attack those who provide new information, and denigrate their published works.
For example, Clarence ‘Sonny’ Williams has personally attacked me and denigrated my published works and my professionalism during the past few years. He is now touting the role of microRNA — as detailed in my model of adaptive evolution of the human brain and behavior — after adamantly touting random mutations theory and other nonsense (e.g., domain specific mental modules; unknown natural mechanisms; lack of transgenerational epigenetic inheritance). Yet his recent post on the importance of microRNA made no mention of the fact that I have detailed its importance. This was done in the model for nutient-dependent pheromone-controlled adaptive evolution that I have extended from microbes to man via their common molecular biology.
I began detailing this with co-authors in our 1996 Hormones and Behavior review article From fertilization to adult sexual behavior. In our section on molecular epigenetics we wrote:
“Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.”
The entirety of this quoted material can be credited to the prescient epigenetic expertise of co-author Teresa Binstock. Thus, the theft of intellectual property by Clarence ‘Sonny’ Williams exemplifies how virtually anyone unethical enough to stake a claim to the decades of collaborative works by others can quite simply assert themselves as an authority with no published works, and no knowledge of anything except random mutations theory. His behavior is unethical and, quite frankly, despicable. However, it serves notice to people like me that unless prepublication formats and venues are used (see: Nutrient-dependent / Pheromone-controlled Adaptive Evolution; Nutrient-dependent / Pheromone-controlled thermodynamics and thermoregulation, virtually anyone can come along and try to take credit for the work of others. Meanwhile, let’s all hope that peer-review actually turns out to be helpful in the second round of review of my February 2013 submission.
