Epigenetics and the Biological Basis of Gene x Environment Interactions
ABSTRACT 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.
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.
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.
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.
- SourceAvailable from: Adam S Wilkins
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- "In particular, the Novosibirsk group has long argued that hormonal states in the mother, associated with the less stressful conditions of domesticity, are involved in generating the DS (Belyaev 1979; Trut et al. 2004, 2009). Findings consistent with this idea, though opposite in effect, involve maternal stresses in mice that create epigenetic chromatin state changes and behavioral phenotypes in offspring (Meany and Szyf 2005; Bagot and Meaney 2010). Whether epimutations have the requisite stability in transgenerational transmission to generate true heritable states is always a key question about their evolutionary potential (Slatkin 2009) but strong trans-generational transmissibility of epigenetic states has been shown for two genes affecting coat color patterns in the mouse, Agouti and Axin Fu genes (Morgan et al. 1999; Rakyan et al. 2003). "
ABSTRACT: Charles Darwin, while trying to devise a general theory of heredity from the observations of animal and plant breeders, discovered that domesticated mammals possess a distinctive and unusual suite of heritable traits not seen in their wild progenitors. Some of these traits also appear in domesticated birds and fish. The origin of Darwin's "domestication syndrome" has remained a conundrum for more than 140 years. Most explanations focus on particular traits, while neglecting others, or on the possible selective factors involved in domestication rather than the underlying developmental and genetic causes of these traits. Here, we propose that the domestication syndrome results predominantly from mild neural crest cell deficits during embryonic development. Most of the modified traits, both morphological and physiological, can be readily explained as direct consequences of such deficiencies, while other traits are explicable as indirect consequences. We first show how the hypothesis can account for the multiple, apparently unrelated traits of the syndrome and then explore its genetic dimensions and predictions, reviewing the available genetic evidence. The article concludes with a brief discussion of some genetic and developmental questions raised by the idea, along with specific predictions and experimental tests.Genetics 07/2014; 197(3):795-808. DOI:10.1534/genetics.114.165423 · 4.87 Impact Factor
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- "On the negative side, there is evidence from multiple lines of research that hippocampal development is profoundly disrupted by negative environmental influences like maternal stress, chronic stress during childhood, and maltreatment (see Farah et al., 2008; Meaney, 2010; Tottenham and Sheridan, 2009). Thanks to extensive research in non-human animals, much is known about the underlying molecular and cellular mechanisms (e.g., Bagot and Meaney, 2010). There is also a growing body of literature indicating that PFC development is affected by chronic stress, intrauterine drug exposure, lead exposure during childhood, and other environmental factors (see Mackey et al., in press). "
ABSTRACT: Episodic memory is central to the human experience. In typically developing children, episodic memory improves rapidly during middle childhood. While the developmental cognitive neuroscience of episodic memory remains largely uncharted, recent research has begun to provide important insights. It has long been assumed that hippocampus-dependent binding mechanisms are in place by early childhood, and that improvements in episodic memory observed during middle childhood result from the protracted development of the prefrontal cortex. We revisit the notion that binding mechanisms are age-invariant, and propose that changes in the hippocampus and its projections to cortical regions also contribute to the development of episodic memory. We further review the role of developmental changes in lateral prefrontal and parietal cortices in this development. Finally, we discuss changes in white matter tracts connecting brain regions that are critical for episodic memory. Overall, we argue that changes in episodic memory emerge from the concerted effort of a network of relevant brain structures.06/2012; 2(4):381-95. DOI:10.1016/j.dcn.2012.05.002
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- "Parental effects occur when the phenotype or experienced environment of one or both parents influences the phenotype of their offspring apart from the effects of direct genetic transmission (Marshall and Uller 2007). Parental effects can be a result of one or both parents influencing offspring phenotypes via nest site selection, nutrient provisioning, hormone transfer, providing particular social experiences or serving as a mentor or model from which to socially learn, and epigenetic modification of gene expression may be an important proximate mechanism (Bagot and Meaney 2010; Crews 2010; Curley et al. 2011). Behavior can act as both a generator and a target of parental effects as parental behaviors may affect nonbehavioral traits in the offspring (for example, parental provisioning behavior may affect offspring size) and nonbehavioral traits in the parents may affect offspring behavior (for example , the deposition of androgens in eggs may increase the aggressiveness of the offspring) (for recent reviews, see Marshall and Uller 2007; Badyaev and Uller 2009; Maestripieri and Mateo 2009; Wolf and Wade 2009). "
ABSTRACT: Parental effects are any effect parents may have on the phenotype of their offspring over and above direct genetic transmission. By adaptively adjusting the phenotypes of their offspring to suit future environmental conditions, parents may increase their own fitness. A likely target of this parental programming is behavior, and the resulting variation in individual behavior can lead to diverse animal personalities. Here, I argue that parental effects may be an important source of variation in behavior and that by synthesizing the fields of parental effects and animal personality, we can gain novel insights into the ecological and evolutionary causes and consequences of individual variation.Behavioral Ecology 03/2012; 23(2-2):242-245. DOI:10.1093/beheco/arr210 · 3.16 Impact Factor