This study investigates the effects of maternal exposure to bisphenol A (BPA), an endocrine-disrupting chemical, on the epigenome of viable yellow agouti (A^vy) mouse offspring. BPA exposure shifted the coat color distribution of offspring towards yellow by decreasing CpG methylation in an intracisternal A particle retrotransposon upstream of the Agouti gene. This effect was also observed at another metastable locus, the CDK5 activator-binding protein (Cebp^IAP). The study found that BPA exposure altered DNA methylation patterns in tissues from all three germ layers, indicating that early stem cell development is sensitive to BPA exposure. Maternal dietary supplementation with methyl donors like folic acid or the phytoestrogen genistein negated the hypomethylating effect of BPA, suggesting that these supplements can counteract the adverse effects of BPA exposure. The findings highlight the importance of maternal nutritional interventions in mitigating the epigenetic alterations caused by environmental contaminants, which can influence adult disease susceptibility.This study investigates the effects of maternal exposure to bisphenol A (BPA), an endocrine-disrupting chemical, on the epigenome of viable yellow agouti (A^vy) mouse offspring. BPA exposure shifted the coat color distribution of offspring towards yellow by decreasing CpG methylation in an intracisternal A particle retrotransposon upstream of the Agouti gene. This effect was also observed at another metastable locus, the CDK5 activator-binding protein (Cebp^IAP). The study found that BPA exposure altered DNA methylation patterns in tissues from all three germ layers, indicating that early stem cell development is sensitive to BPA exposure. Maternal dietary supplementation with methyl donors like folic acid or the phytoestrogen genistein negated the hypomethylating effect of BPA, suggesting that these supplements can counteract the adverse effects of BPA exposure. The findings highlight the importance of maternal nutritional interventions in mitigating the epigenetic alterations caused by environmental contaminants, which can influence adult disease susceptibility.