title: Epigenetics and the biological basis of gene x environment interactions.
abstract: 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.
authors.affiliation: Sackler Program for Epigenetics and Psychobiology, McGill University and Douglas Mental Health University Institute, Montreal, Canada.
authors.forename: Rosemary C
authors.initials: RC
authors.lastname: Bagot
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Meaney
mesh_terms: 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
chemical_list: D005819:Genetic Markers; D011965:Receptors, Glucocorticoid; D000076983:Histone Methyltransferases; D011495:Histone-Lysine N-Methyltransferase