Epigenetics and the biological basis of gene x environment interactions.
OBJECTIVE
Child and adolescent psychiatry is rife with examples of the sustained effects of early experience on brain function. The study of behavioral genetics provides evidence for a relation between genomic variation and personality and with the risk for psychopathology. A pressing challenge is that of conceptually integrating findings from genetics into the study of personality without regressing to arguments concerning the relative importance of genomic variation versus nongenomic or environmental influences.


METHODS
Epigenetics refers to functionally relevant modifications to the genome that do not involve a change in nucleotide sequence. This review examines epigenetics as a candidate biological mechanism for gene x environment interactions, with a focus on environmental influences that occur during early life and that yield sustained effects on neural development and function.


RESULTS
The studies reviewed suggest that epigenetic remodeling occurs in response to the environmental activation of cellular signalling pathways associated with synaptic plasticity, epigenetic marks are actively remodeled during early development in response to environmental events that regulate neural development and function, and epigenetic marks are subject to remodeling by environmental influences even at later stages in development.


CONCLUSIONS
Epigenetic remodeling might serve as an ideal mechanism for phenotypic plasticity--the process whereby the environment interacts with the genome to produce individual differences in the expression of specific traits.
Bagot
Rosemary C
RC
Sackler Program for Epigenetics and Psychobiology, McGill University and Douglas Mental Health University Institute, Montreal, Canada.
Meaney
Michael J
MJ
D000293:Adolescent; D000818:Animals; D002648:Child; D019175:DNA Methylation; D004195:Disease Models, Animal; D044127:Epigenesis, Genetic / Q000235:genetics*; D005786:Gene Expression Regulation / Q000235:genetics; D005819:Genetic Markers / Q000235:genetics; D000076983:Histone Methyltransferases; D011495:Histone-Lysine N-Methyltransferase / Q000235:genetics; D006801:Humans; D007173:Imprinting, Psychological; D008425:Maternal Behavior; D001523:Mental Disorders / Q000235:genetics* / Q000523:psychology*; D010554:Personality Disorders / Q000235:genetics* / Q000523:psychology*; D011965:Receptors, Glucocorticoid / Q000235:genetics; D012307:Risk Factors; D012919:Social Behavior; D012931:Social Environment; D014158:Transcription, Genetic / Q000235:genetics
D005819:Genetic Markers; D011965:Receptors, Glucocorticoid; D000076983:Histone Methyltransferases; D011495:Histone-Lysine N-Methyltransferase