“Transition from Inorganic to Organic Life was Based on [Biological] Information, Not Chemistry” October 15, 2013
Excerpt: “We believe the transition in the informational architecture of chemical networks is akin to a phase transition in physics, and we place special emphasis on the top-down information flow in which the system as a whole gains causal purchase over its components,” Davies added. “This approach will reveal how the logical organization of biological replicators differs crucially from trivial replication associated with crystals (non-life). By addressing the causal role of information directly, many of the baffling qualities of life are explained.”
My comment: There is no experimental evidence that addresses the causal role of biological information in the context of mutation-initiated natural selection. However, in: “The epigenome and top-down causation” P.C. W. Davies wrote: “Epigenetics provides striking examples of how bottom-up genetic and top-down epigenetic causation intermingle.” [sans mutations theory] Thus, it makes as much sense to look for epigenetic top-down cause as it does to look at what is already known about epigenetic cause from the bottom up.
In: “Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors,” I detailed the molecular epigenetics of cause and effect from bottom-up nutrient uptake to top-down pheromone-controlled physiology of reproduction.[sans mutations theory]
In the context of biological information in: “Nutrient-dependent/pheromone-controlled adaptive evolution: a model,” I provided examples of cause and effect in model organisms from microbes to man.[sans mutations theory]
This IS NOT A NEW MODEL of cause and effect. [sans mutations theory] The conserved molecular mechanisms in species from yeasts to mammals were addressed in our section on molecular epigenetics in a 1996 Hormones and Behavior review article: From Fertilization to Adult Sexual Behavior.
“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…. 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…. That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.” [sans mutations theory]
Clearly, if you cannot get to sex differences via mutation-initiated natural selection, you cannot go further with claims of mutation-driven evolution. Thus, if it’s the epigenetics of de novo olfactory receptor gene creation from the bottom up and the epigenetics of top-down control by the de novo creation of species-specific pheromones in one species — as it clearly is in yeast –it’s epigenetics in all species, as detailed in my model.[sans mutations theory]
For example, Schmidt (2013) wrote: “The mechanism by which one signaling pathway regulates a second provides insight into how cells integrate multiple stimuli to produce a coordinated response.” In 1996, we wrote: “Parenthetically it is interesting to note even the yeast Saccharomyces cerevisiae has a gene-based equivalent of sexual orientation (i.e., a-factor and alpha-factor physiologies). These differences arise from different epigenetic modifications of an otherwise identical MAT locus (Runge and Zakian, 1996; Wu and Haber, 1995).” If the nutrient-dependent epigenetic modifications of an otherwise identical MAT locus did not result in a sex difference in pheromone-production in unicellular organisms, mutations might be considered causal to the development of sex differences. However, mutation-initiated natural selection would still not explain the recognition of sex differences in species from microbes to man. Instead, my model of nutrient-dependent pheromone-controlled adaptive evolution includes both the evolution of sex differences, and the concurrent evolution of the ability to recognize sex differences via the nutrient-dependent production of species-specific pheromones that control the physiology of reproduction in all species. And, it is the nutrient-dependent pheromone-controlled physiology of reproduction that explains the diversification of species from microbes to man in my model. [sans mutations theory]
