Development and the epigenome

Development and the epigenome Boyce, W. T., & Kobor, M. S. (2015). Development and the epigenome: The ‘synapse’ of gene– environment interplay. Developmental science, 18(1), 1‐2

Chromatin configuration is con- trolled physicochemically by the placement or removal of chemical tags – i.e. epigenetic ‘marks’, such as methyl, acetyl, phosphate, or ubiquitin groups – on the DNA or histone proteins      —yes, much like software flags

‘histone code’ or ‘histone language’

during mitosis, the pattern of DNA methylation is replicated in daughter cells -> inheritance of state

G–E interplay plays a role in the genesis of species-typical and deviant behavior. Though such evidence had been long anticipated, it was only a decade ago that reports began to emerge documenting G9E interactions in the longitudinal prediction of human developmental and health outcomes.

WOW. Tracing it out.  FKBP5 codes for a so- called ‘chaperone protein’ that alters the function of the glucocorticoid receptor (GR) and impedes the translo- cation of the GR-glucocorticoid complex into the cell nucleus. The demethylation event, which can occur only during an early critical period and results in a persistent activation of FKBP5, then primes the risk allele carrier for stress-induced over-production of the chaperone protein, suppression of GR function, HPA axis dysregulation and a consequent augmentation of risk for PTSD.

‘orchid children’, in contrast to their more resilient counterparts, ‘dandelion children’

epigenetics controls critical periods

Within virtually every contemporary society, the developmental and health effects of early exposures to adversity and stress are socioeconomically partitioned, with children from the lower ranks of social class sustaining greater and more severe threats to normative development; many of these pervasive SES influences on adversity-related, maladaptive outcomes are almost certainly epigenetically mediated.