model of Huntington Disease, lower levels of the H3K4 de-methylase SMCX/Jarid1c have been shown to be neuroprotective, a mechanism that is also conserved in a mouse model (Vashishtha et al., 2013). Contrary to H3K4, methylation at H3K9 is a repressive mark and is involved in alcohol and drugs of abuse phenotypes. Studies reveal a link between G9a (lysine dimethyltransferase), which catalyzes H3K9 methylation, and neurodegeneration in the developing brain that has been exposed to postnatal ethanol, which may have implications for fetal alcohol spectrum disorders (Subbanna et al., 2013). In a chronic ethanol treatment model, both treatment with and withdrawal from ethanol produced an increase in H3K9 acetylation at the NR2B (NMDA receptor 2B) gene promoter and a corresponding decrease in H3K9 methylation (Qiang, Denny, Lieu, Carreon, & Li, 2011). In cultured rat hepatocytes, ethanol decreased the levels of H3K9me2 while concomitantly increasing H3K4me2, with both ultimately contributing to an open chromatin state. This corresponded to increased expression of the alcohol dehydrogenase gene. Furthermore histone H3K9 acetylation was increased in the promoter and coding regions of the gene (Pal-Bhadra et al., 2007; Park et al., 2012). Histone methylation is a dynamic reversible process and is under the control of two
