Multifactorial neurodevelopmental deficit, such as fetal alcohol spectrum disorder (FASD), is likely to occur through gene-environment interactions that alter the fate of early developing precursor cells. Neural stem cells (NSC) are capable of self-renewal and differentiate along neuronal and glial lineages. These processes are defined by the dynamic interplay between extracellular cues, and intracellular transcriptional signaling programs. Recently, epigenetic mechanisms—including DNA methylation, histone modifications, and non-coding RNA expression--have been shown to be closely associated with the fate specification of NSCs. These epigenetic alterations could provide coordinated systems for regulating gene expression at each step of neural cell differentiation. Epigenetic modifications regulate key developmental events, including germ cell imprinting (Bartolomei, 2003), stem cell maintenance (Cheng et al., 2005; Kondo, 2006; Zhang et al., 2006; Meshorer, 2007; Surani et al., 2007; Tang and Zhu, 2007), cell fate, and tissue patterning (Kiefer, 2007). Aberrant epigenetic alterations are known to disrupt key developmental events, particuarly in the nervous system, leading to conditions such as Rett's syndrome (Shahbazian and Zoghbi, 2002), immunodeficiency centromeric instability and facial syndrome (ICF) (Hansen et al., 1999, Tao et al.,
