Transcriptional repression by the SMRT-mSin3 corepressor: Multiple interactions, multiple mechanisms, and a potential role for TFIIB

Chi Wai Wong, Martin L. Privalsky

Research output: Contribution to journalArticle

116 Citations (Scopus)

Abstract

A variety of eukaryotic transcription factors, including the nuclear hormone receptors, Max-Mad, BCL-6, and PLZF, appear to mediate transcriptional repression through the ability to recruit a multiprotein corepressor complex to the target promoter. This corepressor complex includes the SMRT/N-CoR polypeptides, mSin3A or -B, and histone deacetylase 1 or 2. The presence of a histone-modifying activity in the corepressor complex has led to the suggestion that gene silencing is mediated by modification of the chromatin template, perhaps rendering it less accessible to the transcriptional machinery. We report here, however, that the corepressor complex actually appears to exhibit multiple mechanisms of transcriptional repression, only one of which corresponds with detectable recruitment of the histone deacetylase. We provide evidence instead of an alternative pathway of repression that may be mediated by direct physical interactions between components of the corepressor complex and the general transcription factor TFIIB.

Original languageEnglish (US)
Pages (from-to)5500-5510
Number of pages11
JournalMolecular and Cellular Biology
Volume18
Issue number9
StatePublished - 1998

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Nuclear Receptor Co-Repressor 2
Transcription Factor TFIIB
Co-Repressor Proteins
Histone Deacetylase 2
Histone Deacetylase 1
General Transcription Factors
Multiprotein Complexes
Histone Deacetylases
Gene Silencing
Cytoplasmic and Nuclear Receptors
Histones
Chromatin
Transcription Factors
Peptides

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cell Biology

Cite this

Transcriptional repression by the SMRT-mSin3 corepressor : Multiple interactions, multiple mechanisms, and a potential role for TFIIB. / Wong, Chi Wai; Privalsky, Martin L.

In: Molecular and Cellular Biology, Vol. 18, No. 9, 1998, p. 5500-5510.

Research output: Contribution to journalArticle

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