et al., 2009). Drosophila CREB activates expression of the BK-type Ca2+ activated K channel gene (dslo) by binding to the promoter in response to benzyl alcohol sedation leading to a behavioral tolerance to the drug on a subsequent exposure (Wang, Ghezzi, et al., 2009). Furthermore, a mutation in the Drosophila homolog of CBP, nejire (nej), regulates tolerance to benzyl alcohol and ethanol (Ghezzi et al., 2013). Invertebrate models, such as Drosophila, have been invaluable in identifying genetic networks and pathways that regulate disease phenotypes that are conserved between invertebrate and mammalian models due to their forward and reverse genetic approaches (Atkinson, 2009). The identification of conserved epigenetic regulatory networks regulating behaviors related to ethanol exposure in both vertebrates and invertebrates, such as CREB signaling, serve to illustrate the significance of invertebrate genetic models to further our understanding of epigenetic mechanisms of alcoholism.
