An evolving view of epigenetic complexity in the brain
Abstract (with my emphasis): Recent scientific advances have revolutionized our understanding of classical epigenetic mechanisms and the broader landscape of molecular interactions and cellular functions that are inextricably linked to these processes. Our current view of epigenetics includes an increasing appreciation for the dynamic nature of DNA methylation, active mechanisms for DNA demethylation, differential functions of 5-methylcytosine and its oxidized derivatives, the intricate regulatory logic of histone post-translational modifications, the incorporation of histone variants into chromatin, nucleosome occupancy and dynamics, and direct links between cellular signalling pathways and the actions of chromatin ‘reader’, ‘writer’ and ‘eraser’ molecules. We also have an increasing awareness of the seemingly ubiquitous roles played by diverse classes of selectively expressed non-coding RNAs in transcriptional, post-transcriptional, post-translational and local and higher order chromatin modulatory processes. These perspectives are still evolving with novel insights continuing to emerge rapidly (e.g. those related to epigenetic regulation of mobile genetic elements, epigenetic mechanisms in mitochondria, roles in nuclear architecture and ‘RNA epigenetics’). The precise functions of these epigenetic factors/phenomena are largely unknown. However, it is unequivocal that they serve as key mediators of brain complexity and flexibility, including neural development and aging, cellular differentiation, homeostasis, stress responses, and synaptic and neural network connectivity and plasticity.
My comment: The abstract suggests others have finally accepted this fact:
Although the links from epigenetic factors to precise functions associated with affects of hormones on behavior are largely unknown, the epigenetic landscape is clearly linked to the physical landscape of DNA in organized genomes of species from microbes to man via conserved molecular mechanisms.
The conserved molecular mechanisms of protein folding that unequivocally link the epigenetic landscape from ecological variation to nutrient-dependent pheromone-controlled ecological adaptations manifested in behavior in my model eliminate the pseudoscientific nonsense of theories about mutation-initiated natural selection and the evolution of biodiversity.
The only acceptable view of how the epigenetically-effected complexity of the brain arose is presented in my model. My view is that nutrient-dependent pheromone-controlled amino acid substitutions link cell type differentiation in all cells of all tissues in all organs of all organisms with organ systems that include a brain. The link from ecological variation to epigenetic effects of hormones that affect their behavior is clear.
If that link is not considered in the context of a model, it may not be considered in the context of unequivocal facts. And the abstract above would not link the representations in my model of nutrient-dependent pheromone-controlled epigenetic cause and effect to the key mediators of cell type differentiation via amino acid substitutions.
