NSCs with 5-azacytidine (5-AZA), which inhibits DNA methyl transferase, and the new DNA-methylation at the time of differentiation (Matsuda, 1990, Singh et al., 2009b). Retardation of migration, process growth, and key neural phenotype expression were evident. The necessity of methylation programming during embryonic development was also demonstrated by 5-AZA treatment and methionine suppression (methyl donor) resulting in growth retardation and neural tube defect (Dunlevy et al., 2006). Alcohol, known to affect methyl donors, also interferes with the DNA methylation program at early NSC differentiation. In conclusion, using neural stem cells for high-throughput analysis of genome-wide methylation, we demonstrated, for the first time, that alcohol prevented moderately methylated genes from hyper- as well as hypomethylation and affected migration and differentiation of neural stem cells. These results indicate that alcohol alters epigenetic programming while affecting stem-cell-ness and its differentiation. The temporal effect of the alcohol-modified DNA methylation on gene transcription and its causal effect on dysregulation of stem cell development remains under investigation.
