Dot1 and Histone H3K79 Methylation in Natural Telomeric and HM Silencing

Yoh Hei Takahashi, Julia M. Schulze, Jessica Jackson, Thomas Hentrich, Chris Seidel, Sue L. Jaspersen, Michael S. Kobor*, Ali Shilatifard

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

74 Scopus citations

Abstract

The expression of genes residing near telomeres is attenuated through telomere position-effect variegation (TPEV). By using a URA3 reporter located at TEL-VII-L of Saccharomyces cerevisiae, it was proposed that the disruptor of telomeric silencing-1 (Dot1) regulates TPEV by catalyzing H3K79 methylation. URA3 reporter assays also indicated that H3K79 methylation is required for HM silencing. Surprisingly, a genome-wide expression analysis of H3K79 methylation-defective mutants identified only a few telomeric genes, such as COS12 at TEL-VII-L, to be subject to H3K79 methylation-dependent natural silencing. Consistently, loss of Dot1 did not globally alter Sir2 or Sir3 occupancy in subtelomeric regions, but only led to some telomere-specific changes. Furthermore, H3K79 methylation by Dot1 did not play a role in the maintenance of natural HML silencing. Therefore, commonly used URA3 reporter assays may not report on natural PEV, and therefore, studies concerning the epigenetic mechanism of silencing in yeast should also employ assays reporting on natural gene expression patterns.

Original languageEnglish (US)
Pages (from-to)118-126
Number of pages9
JournalMolecular cell
Volume42
Issue number1
DOIs
StatePublished - Apr 8 2011

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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