Rest repression of neuronal genes requires components of the hSWI·SNF complex

Elena Battaglioli, Maria E. Andrés, Dave W. Rose, Josh G. Chenoweth, Michael G. Rosenfeld, Mary E. Anderson, Gail Mandel

Research output: Contribution to journalArticlepeer-review

161 Scopus citations

Abstract

A function of the transcription factor REST is to block the expression of neuronal phenotypic traits in nonneuronal cells. Previous studies have shown that REST-mediated repression requires histone deacetylase activity and that recruitment of deacetylases is mediated by two co-repressors, Sin3A and CoREST. In this study, we show that a repressor domain in CoREST interacts with BRG1-associated factor (BAF) 57, a component of the hSWI·SNF complex. In vivo, BAF57 occupies the neuronal sodium channel gene (Nav1.2) promoter, and targeting to this gene requires REST. In addition to BAF57, the ATPase BRG1 and BAF170, other members of the hSWI·SNF complex, are also present in the REST·CoREST repressor complex. Microinjection of specific antibodies against BRG1, BAF57, or BAF170 into Rat1 fibroblasts relieves repression of RE1 reporter genes. Together, our data suggest that ATP-dependent chromatin remodeling, as well as histone deacetylation, is needed for REST-mediated repression.

Original languageEnglish (US)
Pages (from-to)41038-41045
Number of pages8
JournalJournal of Biological Chemistry
Volume277
Issue number43
DOIs
StatePublished - Oct 25 2002
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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