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. 2021 Nov 29;53(11):1683–1688. doi: 10.1038/s12276-021-00711-x

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© The Author(s) 2021

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. 1 — The Paf1 complex, Bur1/Bur2 and Kin28 kinases, and N-terminal tails of H2A facilitate H2B monoubiquitination (ub) during yeast transcription. H2Bub then promotes H3K4 and H3K79 methylation (me) both directly and via the proteasomal ATPases Rpt4 and Rpt6. H3R2me mutually antagonizes H3K4me, whereas H4R3me interferes with the binding ability of H3K4 methyltransferase (no reports of H4R3me in S. cerevisiae). Although either H2Bub- or H3K4me-stimulated histone (poly)sumoylation blocks the recruitment of Ctk1 CTDS2 kinase, facilitating H3K36me modification for loading of the Rpd3S HDAC complex, both H3K4me and histone (poly)sumoylation are required for the chromatin binding of the Set3 HDAC complex.