Maternal nutrient supplementation counteracts bisphenol A (BPA)-induced DNA hypomethylation in early development. This study shows that maternal exposure to BPA shifts the coat color distribution of viable yellow agouti (A^vy) mouse offspring toward yellow by decreasing CpG methylation in an intracisternal A particle retrotransposon upstream of the Agouti gene. CpG methylation was also decreased at another metastable locus, the CDK5 activator-binding protein (Cabp^IAP). DNA methylation at the A^vy locus was similar in tissues from the three germ layers, providing evidence that epigenetic patterning during early stem cell development is sensitive to BPA exposure. Moreover, maternal dietary supplementation with methyl donors like folic acid or the phytoestrogen genistein negated the DNA hypomethylating effect of BPA. Thus, the study presents compelling evidence that early developmental exposure to BPA can change offspring phenotype by stably altering the epigenome, an effect that can be counteracted by maternal dietary supplements. The study used the A^vy mouse model to evaluate how the fetal epigenome is affected by maternal exposure to the estrogenic xenobiotic chemical BPA. BPA is a high production volume chemical used in the manufacture of polycarbonate plastic and epoxy resins. It is present in many commonly used products including food and beverage containers, baby bottles, and dental composites. The detection of BPA in 95% of human urine samples clearly attests to the widespread use of BPA and widespread human exposure to BPA. Rodent studies have associated pre- or perinatal BPA exposure with higher body weight, increased breast and prostate cancer, altered reproductive function, and other chronic health effects. BPA also enters the placenta and accumulates in fetuses after rodent maternal oral exposure. Herein, we report the effect of maternal BPA exposure alone or in combination with nutritional supplements on the epigenome of the offspring. Maternal dietary BPA did not significantly influence litter size, survival, wean weight, genotypic ratio, or sex ratio. In contrast, maternal BPA significantly shifted the coat color distribution of genetically identical offspring toward the yellow coat color phenotype. Maternal supplementation with methyl donors or genistein restored the coat color distribution in BPA-exposed offspring to that observed in control litters. Maternal nutritional supplementation also negated the BPA-induced DNA hypomethylation in the offspring. The study shows that maternal dietary exposure to BPA markedly alters the adult phenotype of the offspring by hypomethylating the epigenome. Maternal nutritional supplementation with methyl donors or genistein counteracts BPA-induced hypomethylation, resulting in a control coat color distribution in the BPA-exposed offspring. BPA is ubiquitously present in the human population, so these findings hold promise for reducing disease susceptibilityMaternal nutrient supplementation counteracts bisphenol A (BPA)-induced DNA hypomethylation in early development. This study shows that maternal exposure to BPA shifts the coat color distribution of viable yellow agouti (A^vy) mouse offspring toward yellow by decreasing CpG methylation in an intracisternal A particle retrotransposon upstream of the Agouti gene. CpG methylation was also decreased at another metastable locus, the CDK5 activator-binding protein (Cabp^IAP). DNA methylation at the A^vy locus was similar in tissues from the three germ layers, providing evidence that epigenetic patterning during early stem cell development is sensitive to BPA exposure. Moreover, maternal dietary supplementation with methyl donors like folic acid or the phytoestrogen genistein negated the DNA hypomethylating effect of BPA. Thus, the study presents compelling evidence that early developmental exposure to BPA can change offspring phenotype by stably altering the epigenome, an effect that can be counteracted by maternal dietary supplements. The study used the A^vy mouse model to evaluate how the fetal epigenome is affected by maternal exposure to the estrogenic xenobiotic chemical BPA. BPA is a high production volume chemical used in the manufacture of polycarbonate plastic and epoxy resins. It is present in many commonly used products including food and beverage containers, baby bottles, and dental composites. The detection of BPA in 95% of human urine samples clearly attests to the widespread use of BPA and widespread human exposure to BPA. Rodent studies have associated pre- or perinatal BPA exposure with higher body weight, increased breast and prostate cancer, altered reproductive function, and other chronic health effects. BPA also enters the placenta and accumulates in fetuses after rodent maternal oral exposure. Herein, we report the effect of maternal BPA exposure alone or in combination with nutritional supplements on the epigenome of the offspring. Maternal dietary BPA did not significantly influence litter size, survival, wean weight, genotypic ratio, or sex ratio. In contrast, maternal BPA significantly shifted the coat color distribution of genetically identical offspring toward the yellow coat color phenotype. Maternal supplementation with methyl donors or genistein restored the coat color distribution in BPA-exposed offspring to that observed in control litters. Maternal nutritional supplementation also negated the BPA-induced DNA hypomethylation in the offspring. The study shows that maternal dietary exposure to BPA markedly alters the adult phenotype of the offspring by hypomethylating the epigenome. Maternal nutritional supplementation with methyl donors or genistein counteracts BPA-induced hypomethylation, resulting in a control coat color distribution in the BPA-exposed offspring. BPA is ubiquitously present in the human population, so these findings hold promise for reducing disease susceptibility