Chromatin signaling to kinetochores: Transregulation of Dam1 methylation by histone H2B ubiquitination

John A. Latham, Renée J. Chosed, Shanzhi Wang, Sharon Y.R. Dent

Research output: Contribution to journalArticlepeer-review

55 Scopus citations

Abstract

Histone H3K4 trimethylation by the Set1/MLL family of proteins provides a hallmark for transcriptional activity from yeast to humans. In S. cerevisiae, H3K4 methylation is mediated by the Set1-containing COMPASS complex and is regulated in trans by prior ubiquitination of histone H2BK123. All of the events that regulate H2BK123ub and H3K4me are thought to occur at gene promoters. Here we report that this pathway is indispensable for methylation of the only other known substrate of Set1, K233 in Dam1, at kinetochores. Deletion of RAD6, BRE1, or Paf1 complex members abolishes Dam1 methylation, as does mutation of H2BK123. Our results demonstrate that Set1-mediated methylation is regulated by a general pathway regardless of substrate that is composed of transcriptional regulatory factors functioning independently of transcription. Moreover, our data identify a node of regulatory crosstalk in trans between a histone modification and modification on a nonhistone protein, demonstrating that changing chromatin states can signal functional changes in other essential cellular proteins and machineries.

Original languageEnglish (US)
Pages (from-to)709-719
Number of pages11
JournalCell
Volume146
Issue number5
DOIs
StatePublished - Sep 2 2011

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology

MD Anderson CCSG core facilities

  • Advanced Technology Genomics Core

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