Epigenetic profiling in adult brain after prenatal BPA exposure [ChIP-seq]

We reported that, in C57BL/6Slac mice, prenatally exposure to low-dose BPA induces up-regulation of genes associated with neuronal function and down-regulation of genes related to mitochondrial oxidative phosphorylation. Three-dimensional chromatin organization of these differential expressed genes revealed that up-regulated genes are primarily under control of remote enhancers, while down-regulated genes appear to be regulated by chromatin interactions among relative adjacent genes. Further examination of genome-wide repressive epigenetic modifications, specifically DNA methylation, H3K27me3, and H3K9me3 revealed that transcription of down-regulated genes might be repressed directly by enhanced DNA methylation and H3K27me3 modifications at promoter regions and indirectly by increased DNA methylation at their corresponding interaction regions, while up-regulated genes might be regulated by loss of H3K9me3 occupancy on distal regulatory regions. Examination of histone H3K9me3 and H3K27me3 modification in of adult male cortex.