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Variation in GATA1 Moderates the Association Between Childhood Adversity and Amygdala Habituation
Research Mentor and Department
Early life stress is amongst the strongest predictors of depression. Research suggests that stress might disrupt synaptic plasticity as well as brain structure and function. Because GATA1 suppresses the expression of synaptic-function-related genes, stress-induced increase in GATA1 expression is one potential etiologic mechanism underlying the depressogenic effects of stress. Genetic and neuroimaging data were available from 322 participants who completed the Duke Neurogenetics Study, an ongoing protocol assessing a wide range of behavioral and biological phenotypes among young adult volunteers. We examined whether genetic variation in the only GATA1 SNP on our genome-wide array, rs5906709, moderates the effects of childhood adversity on threat-related amygdala habituation, a neural phenotype linked to reduced stress reactivity. GATA1 genotype interacted with childhood adversity to predict amygdala habituation in the left dorsal and ventral amygdala (ps<0.003). Post hoc testing showed that minor allele carriers had reduced left amygdala habituation in the context of elevated childhood adversity (p=0.01), while there was no relationship in major allele homozygotes. Because increased amygdala habituation has been linked to more adaptive responses to stressors, these data suggest that minor allele carriers at rs5906709, may be more susceptible to stress-related psychopathology, including mood and anxiety disorders.