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. 2018 Jun 4;12:1179069518779809. doi: 10.1177/1179069518779809

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© The Author(s) 2018

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 1. — Schematic model of the role of epigenetic modifiers in functional tolerance. The figure shows the transition from a transcriptionally silent, condensed chromatin state (top) to a transcriptionally active, relaxed chromatin state (bottom) during the development of functional alcohol tolerance. (1) The histone acetyltransferase CBP, which is induced by alcohol, catalyzes the addition of acetyl groups to the tails of histone H3 and H4, resulting in the relaxation of chromatin and promoting alcohol tolerance. Mutations in CBP reduce alcohol tolerance. (2) The histone deacetylase SIRT1, which is suppressed by alcohol, catalyzes the removal of acetyl groups from the tails of histone H3, resulting in chromatin condensation and reduces alcohol resistance. Mutations in SIRT1 enhance alcohol tolerance. (3) The histone demethylases NO66 and LID catalyze the removal of activating methyl groups from the tails of histone H3 residues K4 and K36, resulting in chromatin condensation and reduce alcohol resistance. Mutations in NO66 and LID enhance alcohol tolerance. (4) The histone demethylase KDM3 catalyzes the addition of repressive methyl groups from the tails of histone H3 residue K9, resulting in the relaxation of chromatin and favoring alcohol tolerance. Mutations in KDM3 reduce alcohol tolerance.