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. 2019 Sep 19;10:4270. doi: 10.1038/s41467-019-12077-w

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — Model for the regulation of histone acetylation by Hda1C. At hyperactive genes, Hda1C strongly interacts with RNA Pol II to specifically deacetylate histone H4 within coding regions. Deacetylation of H4 by Hda1C may inhibit RNA Pol II elongation. At genes transcribing at intermediate levels, both Hda1C and Rpd3S promote histone deacetylation. When a gene is currently transcribing, Hda1C interacting with RNA Pol II may deacetylate histone H4. When a gene is not being transcribed, or once RNA Pol II passes, recognition of H3K36me3 by the Eaf3 chromodomain of Rpd3S may result in deacetylation of the remaining acetylated histones. Both Hda1C and Rpd3S may negatively affect elongation. In addition, Rpd3S inhibits initiation from cryptic promoters and suppresses histone exchange. At inactive or inducible genes, Hda1C preferentially deacetylates histone H3 to delay the kinetics of gene induction