This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Sullivan, M.
Right arrow Articles by Morgan, D. O.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sullivan, M.
Right arrow Articles by Morgan, D. O.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, September 2008, p. 5328-5336, Vol. 28, No. 17
0270-7306/08/$08.00+0     doi:10.1128/MCB.00235-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Cyclin-Specific Control of Ribosomal DNA Segregation{triangledown}

Matt Sullivan, Liam Holt, and David O. Morgan*

Departments of Physiology and Biochemistry & Biophysics, University of California, San Francisco, California

Received 12 February 2008/ Returned for modification 28 March 2008/ Accepted 24 June 2008

Following chromosome duplication in S phase of the cell cycle, the sister chromatids are linked by cohesin. At the onset of anaphase, separase cleaves cohesin and thereby initiates sister chromatid separation. Separase activation results from the destruction of its inhibitor, securin, which is triggered by a ubiquitin ligase called the anaphase-promoting complex (APC). Here, we show in budding yeast that securin destruction and, thus, separase activation are not sufficient for the efficient segregation of the repetitive ribosomal DNA (rDNA). We find that rDNA segregation also requires the APC-mediated destruction of the S-phase cyclin Clb5, an activator of the protein kinase Cdk1. Mutations that prevent Clb5 destruction are lethal and cause defects in rDNA segregation and DNA synthesis. These defects are distinct from the mitotic-exit defects caused by stabilization of the mitotic cyclin Clb2, emphasizing the importance of cyclin specificity in the regulation of late-mitotic events. Efficient rDNA segregation, both in mitosis and meiosis, also requires APC-dependent destruction of Dbf4, an activator of the protein kinase Cdc7. We speculate that the dephosphorylation of Clb5-specific Cdk1 substrates and Dbf4-Cdc7 substrates drives the resolution of rDNA in early anaphase. The coincident destruction of securin, Clb5, and Dbf4 coordinates bulk chromosome segregation with segregation of rDNA.


* Corresponding author. Mailing address: UCSF Mailcode 2200, Genentech Hall Room N312B, 600 16th Street, San Francisco, CA 94158-2517. Phone: (415) 476-6695. Fax: (415) 476-5233. E-mail: David.Morgan{at}ucsf.edu

{triangledown} Published ahead of print on 30 June 2008.


Molecular and Cellular Biology, September 2008, p. 5328-5336, Vol. 28, No. 17
0270-7306/08/$08.00+0     doi:10.1128/MCB.00235-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.