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Molecular and Cellular Biology, September 1998, p. 5500-5510, Vol. 18, No. 9
Section of Microbiology, Division of
Biological Sciences, University of California at Davis, Davis,
California 95616
Received 22 January 1998/Returned for modification 10 March
1998/Accepted 11 June 1998
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.
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Transcriptional Repression by the SMRT-mSin3
Corepressor: Multiple Interactions, Multiple Mechanisms, and a
Potential Role for TFIIB
*
Corresponding author. Mailing address: Section of
Microbiology, Division of Biological Sciences, One Shields Ave.,
University of California at Davis, Davis, CA 95616. Phone: (530)
752-3013. Fax: (530) 752-9014. E-mail:
mlprivalsky{at}ucdavis.edu.
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