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MBC in Press, published online ahead of print July 7, 2004
Mol. Biol. Cell 10.1091/mbc.E04-05-0412

A more recent version of this article appeared on September 1, 2004
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Submitted on May 18, 2004
Revised on June 15, 2004
Accepted on June 22, 2004

Promoter-Dependent Roles for the Srb10 Cyclin-Dependent Kinase and the Hda1 Deacetylase in Tup1-Mediated Repression in Saccharomyces cerevisiae

Sarah R. Green* and Alexander D. Johnson*{dagger}{ddagger}

*Department of Biochemistry and Molecular Biology and {dagger}Department of Microbiology and Immunology, University of California-San Francisco, San Francisco, CA 94143

Monitoring Editor: David Botstein

The Ssn6-Tup1 complex has been well characterized as a S. cerevisiae general transcriptional repressor with functionally conserved homologues in metazoans. These homologues are essential for cell differentiation and many other developmental processes. The mechanism of repression of all of these proteins remains poorly understood. Srb10 (a cyclin/CDK associated with the Mediator complex) and Hda1 (a class I histone deacetylase) have each been implicated in Tup1-mediated repression. We present a statistically based genome-wide analysis that reveals that Hda1 partially represses roughly 30% of Tup1-repressed genes, whereas Srb10 kinase activity contributes to the repression of ~15% of Tup1-repressed genes. These effects only partially overlap, suggesting that different Tup1-repression mechanisms predominate at different promoters. We also demonstrate a distinction between histone deacetylation and transcriptional repression. In an HDA1 deletion, many Tup1-repressed genes are hyperacetylated at lysine 18 of histone H3, yet are not derepressed, indicating deacetylation alone is not sufficient to repress most Tup1-controlled genes. In a strain lacking both Srb10 and Hda1 functions, over half of the Tup1-repressed genes are still repressed, suggesting that Tup1-mediated repression occurs by multiple, partially overlapping mechanisms, at least one of which is unknown.

{ddagger}Corresponding author. E-mail: ajohnson{at}cgl.ucsf.edu






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