H2AX controls motor learning and response to oxidative stress

ATM drives DNA repair through rapid phosphorylation of the histone variant H2AX. Similarities between ATM and H2AX are evident in the phenotypes of their knockout mouse models, but the role of H2AX in the brain remains obscure. Here, we provide the first evidence that H2AX loss leads to neurobehavioral deficits. H2AX regulates proper response to oxidative stress through Nrf2-transcriptional targets and treatment with antioxidant ameliorates the neurobehavioral deficits. 6 samples in total including 3 replicates of parental mouse embryonic fibroblasts (MEF) and 3 replicates of H2AX knockout MEF.