Gene expression and its discontents: Developmental disorders as dysfunctions of epigenetic cognition

Abstract

Reductionist treatments of the epigenetic regulation of gene expression suffer the same mereological and sufficiency fallacies that haunt both contemporary systems biology and neural network models of high order cognition. Shifting perspective from the massively parallel space of gene matrix interactions to the grammar/syntax of the time series of developmentally expressed phenotypes using a cognitive paradigm permits import of techniques from statistical physics via the homology between information source uncertainty and free energy density. This produces a broad spectrum of 'coevolutionary' probability models of development and its pathologies in which epigenetic regulation and the effects of embedding environment are analogous to a tunable enzyme catalyst. A cognitive paradigm naturally incorporates memory, leading directly to models of epigenetic inheritance, as affected by environmental exposures, in the largest sense. Understanding gene expression, development, and their dysfunctions will require data analysis tools considerably more sophisticated than the present crop of simplistic models abducted from neural network studies or stochastic chemical reaction theory.