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Chunk #21 — Prenatal Alcohol Exposure — DNA methylation

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Epigenetic mechanisms in alcohol- and adversity-induced developmental origins of neurobehavioral functioning.
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of cells produced by the stem cell population (Zhou et al., 2011). Reduced differentiation potential occurred alongside changes to methylation patterns during stem cell progression through the cell cycle. Mukhopadhyay et al. (2013) reported decreased global methylation in cultured mouse embryonic fibroblasts, as well as reduced levels of DNA methyltransferases and MeCP2. Taken together, these studies demonstrate that alcohol affects methylation of genes involved in cell cycle progression, though the direction of these changes could depend on factors including cell type, treatment paradigm, and timing of analysis after exposure, as Liyanage et al. (2015) reported differences in methylation status between alcohol exposure and withdrawal. Cell cycle genes were also associated with increased methylation in a whole embryo culture paradigm (Liu et al., 2009). Most importantly, hypermethylation of chromosomes 10 and X was reported to occur at higher rates in alcohol-exposed embryos displaying physical dysmorphologies related to neural tube defects compared to unaffected embryos, illustrating a link between methylation patterns and alcohol-induced malformations.