The epigenetics of emergent phenotypes
March 25, 2013 | James Kohl
The genetics of emergent phenotypes
Excerpt: “Concepts of emergence range from the mundane (the whole is more than the sum of its parts) to the magical (where the behaviour of a system is not reducible to or predictable from the state and interactions of all its components, and where new properties emerge apparently “for free”). In fact, it is possible to allow for new principles and properties at higher levels without invoking such mystical concepts or over-riding the fundamental laws of physics.
Nature is organised hierarchically into systems at different levels. Subatomic particles are arranged as atoms, atoms into molecules, molecules in cells, cells into tissues and organs, and ultimately organisms, individual organisms in collectives and societies. At each level, qualitatively novel properties arise from the collective action of the components at the level below.”
My comment: The gene, cell, tissue, organ, organ system pathway of organisms epigenetically links sensory input to genetically predisposed phenotypes in my model.
Phenotypic expression ’emerges’ via the epigenetic effects of nutrients, which metabolize to pheromones that control reproduction. The pre-existing pleiotropy of nutrient-dependent genetic predisposition enables adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction. Organism-level epistasis is ecologically achieved and socially maintained in microbes that adaptively evolve to nematodes with their primitive neurogenic niches, and to insects like the honeybee with its hormone-organized and hormone-activated socio-cognitive niche. The adaptive evolution of the hormone-organized and hormone-activated socio-cognitive niche in eusocial organisms like the honeybee, perfectly predicts and also explains the emergence of our nutrient-dependent pheromone-controlled socio-cognitive niche.
The epigenetic landscape becomes the physical landscape of our DNA in cells that include the hormone-secreting nerve cells of the brain that enable the epigenetic effects of food odors and pheromones to rewire the development of our brain and behavior throughout our life cycle transitions. In this context, we are rewired by experience just like honeybees are rewired by experience.
Kevin Mitchell attributes gene expression and protein interactions to thermodynamic noise at the molecular level and to random mutations that cause disordered mental development. Perhaps inadvertently, he also attributes the genetically predisposed diversity of phenotypic expression that results in species-specific epistasis to “noise” and to random mutations.
In my model, for comparison, the precisely controlled nutrient-dependent thermodynamics of intracellular signaling and stochastic gene expression enables organism-level thermoregulation in species from microbes to man. I could attribute the thermodynamics and thermoregulation to noise and random mutations if there was no need to address the systems biology that must be modeled in species from microbes to man before anything can be described as an emergent phenotype.