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Molecular and Cellular Biology, May 2006, p. 3889-3901, Vol. 26, No. 10
0270-7306/06/$08.00+0     doi:10.1128/MCB.26.10.3889-3901.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Role of Histone Deacetylase Rpd3 in Regulating rRNA Gene Transcription and Nucleolar Structure in Yeast

Melanie L. Oakes,^1, Imran Siddiqi,^1,, Sarah L. French,² Loan Vu,¹ Manabu Sato,¹ John P. Aris,³ Ann L. Beyer,² and Masayasu Nomura^1*

Department of Biological Chemistry, University of California—Irvine, Irvine, California 92697-1700,¹ Department of Microbiology, University of Virginia Health System, Charlottesville, Virginia 22908-0734,² Department of Anatomy and Cell Biology, University of Florida, Gainesville, Florida 32610-0235³

Received 30 August 2005/ Returned for modification 31 October 2005/ Accepted 6 March 2006

The 35S rRNA genes at the RDN1 locus in Saccharomyces cerevisiae can be transcribed by RNA polymerase (Pol) II in addition to Pol I, but Pol II transcription is usually silenced. The deletion of RRN9 encoding an essential subunit of the Pol I transcription factor, upstream activation factor, is known to abolish Pol I transcription and derepress Pol II transcription of rRNA genes, giving rise to polymerase switched (PSW) variants. We found that deletion of histone deacetylase gene RPD3 inhibits the appearance of PSW variants in rrn9 deletion mutants. This inhibition can be explained by the observed specific inhibition of Pol II transcription of rRNA genes by the rpd3 mutation. We propose that Rpd3 plays a role in the maintenance of an rRNA gene chromatin structure(s) that allows Pol II transcription of rRNA genes, which may explain the apparently paradoxical previous observation that rpd3 mutations increase, rather than decrease, silencing of reporter Pol II genes inserted in rRNA genes. We have additionally demonstrated that Rpd3 is not required for inhibition of Pol I transcription by rapamycin, supporting the model that Tor-dependent repression of the active form of rRNA genes during entry into stationary phase is Rpd3 independent.

M.L.O. and I.S. contributed equally to this work.

Present address: Department of Anatomic Pathology, University of California—San Francisco, San Francisco, CA 94143.

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