한빛사 논문
Hyun Jin Bae1,6, Marion Dubarry2,6, Jongcheol Jeon1,3, Luis M. Soares1,5, Catherine Dargemont4, Jaehoon Kim3, Vincent Geli2,* & Stephen Buratowski1,*
1 Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA. 2 Cancer Research Center of Marseille (CRCM), U1068 Inserm, UMR7258 CNRS, Aix Marseille University (AMU), Institut Paoli-Calmettes. Equipe labellisée Ligue contre le cancer, Marseille 13009, France. 3 Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 34141, South Korea. 4 Institute of Human Genetics, UMR 9002 CNRS, Montpellier 34396, France. 5Present address: Foghorn Therapeutics, Cambridge, MA 02142, USA. 6These authors contributed equally: Hyun Jin Bae, Marion Dubarry.
*Corresponding author
Abstract
Methylation of histone H3 lysine 4 (H3K4) by Set1/COMPASS occurs co-transcriptionally, and is important for gene regulation. Set1/COMPASS associates with the RNA polymerase II C-terminal domain (CTD) to establish proper levels and distribution of H3K4 methylations. However, details of CTD association remain unclear. Here we report that the Set1 N-terminal region and the COMPASS subunit Swd2, which interact with each other, are both needed for efficient CTD binding in Saccharomyces cerevisiae. Moreover, a single point mutation in Swd2 that affects its interaction with Set1 also impairs COMPASS recruitment to chromatin and H3K4 methylation. A CTD interaction domain (CID) from the protein Nrd1 can partially substitute for the Set1 N-terminal region to restore CTD interactions and histone methylation. However, even when Set1/COMPASS is recruited via the Nrd1 CID, histone H2B ubiquitylation is still required for efficient H3K4 methylation, indicating that H2Bub acts after the initial recruitment of COMPASS to chromatin.
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