Molecules and Cells

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Fig. 2. Hda1C differentially deacetylates histone H4 and H3, depending on transcription frequency. (A) Hda1C is recruited to hyperactive genes via its interaction with elongating RNA Pol II, RNA transcripts, and histones. This complex selectively deacetylates histone H4 at coding regions of hyperactive genes to negatively regulate RNA Pol II elongation. In contrast, Hda1C functionally and physically interacts with Tup1 corepressor to preferentially deacetylate histone H3 and repress transcription of stress response genes. (B) Hda1C and the Set2-Rpd3S pathway collaborate to maintain optimal histone acetylation within coding regions and may function at different times on the same genes. Hda1C deacetylates histone H4 at actively transcribing genes through the interaction with elongating RNA Pol II. In contrast, Rpd3S HDAC may deacetylate histones via recognition of H3K36 methylation when the genes are not currently transcribing by RNA Pol II.
Mol. Cells 2020;43:841~847
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