Anti-silencing factor epe1 associates with SAGA to regulate transcription within heterochromatin

Kehan Bao, Chun Min Shan, James Moresco, John Yates, Songtao Jia

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


Heterochromatin is a highly condensed form of chromatin that silences gene transcription. Although high levels of transcriptional activities disrupt heterochromatin, transcription of repetitive DNA elements and subsequent processing of the transcripts by the RNAi machinery are required for heterochromatin assembly. In fission yeast, a JmjC domain protein, Epe1, promotes transcription of DNA repeats to facilitate heterochromatin formation, but overexpression of Epe1 leads to heterochromatin defects. However, the molecular function of Epe1 is not well understood. By screening the fission yeast deletion library, we found that heterochromatin defects associated with Epe1 overexpression are alleviated by mutations of the SAGA histone acetyltransferase complex. Overexpressed Epe1 associates with SAGA and recruits SAGA to heterochromatin regions, which leads to increased histone acetylation, transcription of repeats, and the disruption of heterochromatin. At its normal expression levels, Epe1 also associates with SAGA, albeit weakly. Such interaction regulates histone acetylation levels at heterochromatin and promotes transcription of repeats for heterochromatin assembly. Our results also suggest that increases of certain chromatin protein levels, which frequently occur in cancer cells, might strengthen relatively weak interactions to affect the epigenetic landscape.

Original languageEnglish (US)
Pages (from-to)116-126
Number of pages11
JournalGenes and Development
Issue number1-2
StatePublished - Jan 1 2019
Externally publishedYes


  • Epe1
  • Heterochromatin
  • Histone
  • Methylation
  • SAGA
  • Transcription

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology


Dive into the research topics of 'Anti-silencing factor epe1 associates with SAGA to regulate transcription within heterochromatin'. Together they form a unique fingerprint.

Cite this