Poster title: From hydrogen-atom transfer in DNA base pairs to ecosystems (March 16-17, 2016)
Abstract: This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on DNA base pairs in solution and RNA-mediated amino acid substitutions to chromosomal rearrangements via pheromone-controlled changes in the microRNA / messenger RNA balance. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent & pH-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Critical limits for enhanced medical care already include what is known about the RNA-mediated physics and chemistry of biologically-based ecological, social, neurogenic and socio-cognitive niche construction. The epigenetic landscape is clearly linked to the physical landscape of supercoiled DNA and top-down causation is manifested in increasing organismal complexity in species from microbes to humans. In all vertebrates and invertebrates the reciprocal relationships of species-typical nutrient-dependent & pH-dependent morphological and behavioral diversity are enabled by microRNAs, adhesion proteins, and pheromone-controlled reproduction. Ecological variation and biophysically constrained natural selection of nutrients cause the RNA-mediated behaviors that enable ecological adaptations, which include development of the brain during life history transitions. Ideas from population genetics typically exclude ecological factors, which must be linked to cell type differentiation. Theories are integrated with an experimental evidence-based approach that establishes what is currently known in the context of this mammalian model.
Today [2/3/16] at 3:05 pm
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…will present evidence that the “social environment” early in life can alter DNA methylation, the basis for the emerging field of “social epigenetics”. By highlighting the impact that external factors and the social environment can have on gene expression, he will provide a mechanistic basis for the long term effects of early childhood experience.
My comment: It will be interesting to compare notes from the Virtual Event to notes from the AAAS Symposium in the context of these publications.
…the nature/nurture debate is much more than simply a scientific argument. It is a clash of cultures, of ideologies and of politics.
The impact of epigenetic effects of chemical ecology on behavioral affects is now relatively well-known (Ledón-Rettig et al., 2012). Effects on hormones and their affects on behavior have been detailed in the honeybee model organism. ‘The concept that is extended is the epigenetic tweaking of immense gene networks in “superorganisms” that “solve problems through the exchange and the selective cancellation and modification of signals”’ (references in Kohl, 2012).
In this emerging paradigm, mitochondria lie at the interface of genetic and environmental factors contributing to disease trajectories.
Using both WT mice and a humanized mouse model of reduced BDNF function (Val66Met SNP), we found that the epigenetic activator of histone acetylation, P300, plays a pivotal role in the dynamic up- and down-regulation of mGlu2 expression in the hippocampus in response to chronic and acute novel and familiar stressors.