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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Liang, F.
Right arrow Articles by Wang, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Liang, F.
Right arrow Articles by Wang, Y.

Next Article 

Molecular and Cellular Biology, July 2007, p. 5067-5078, Vol. 27, No. 14
0270-7306/07/$08.00+0     doi:10.1128/MCB.00095-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

DNA Damage Checkpoints Inhibit Mitotic Exit by Two Different Mechanisms{triangledown}

Fengshan Liang and Yanchang Wang*

Department of Biomedical Sciences, College of Medicine, Florida State University, 1115 West Call Street, Tallahassee, Florida 32306

Received 16 January 2007/ Returned for modification 15 February 2007/ Accepted 30 April 2007

Cyclin-dependent kinase (CDK) governs cell cycle progression, and its kinase activity fluctuates during the cell cycle. Mitotic exit pathways are responsible for the inactivation of CDK after chromosome segregation by promoting the release of a nucleolus-sequestered phosphatase, Cdc14, which antagonizes CDK. In the budding yeast Saccharomyces cerevisiae, mitotic exit is controlled by the FEAR (for "Cdc-fourteen early anaphase release") and mitotic exit network (MEN) pathways. In response to DNA damage, two branches of the DNA damage checkpoint, Chk1 and Rad53, are activated in budding yeast to prevent anaphase entry and mitotic exit, allowing cells more time to repair damaged DNA. Here we present evidence indicating that yeast cells negatively regulate mitotic exit through two distinct pathways in response to DNA damage. Rad53 prevents mitotic exit by inhibiting the MEN pathway, whereas the Chk1 pathway prevents FEAR pathway-dependent Cdc14 release in the presence of DNA damage. In contrast to previous data, the Rad53 pathway negatively regulates MEN independently of Cdc5, a Polo-like kinase essential for mitotic exit. Instead, a defective Rad53 pathway alleviates the inhibition of MEN by Bfa1.

* Corresponding author. Mailing address: Department of Biomedical Sciences, College of Medicine, Florida State University, 1115 West Call Street, Tallahassee, FL 32306. Phone: (850) 644-0402. Fax: (850) 644-5781. E-mail: yanchang.wang{at}med.fsu.edu

{triangledown} Published ahead of print on 7 May 2007.

Molecular and Cellular Biology, July 2007, p. 5067-5078, Vol. 27, No. 14
0270-7306/07/$08.00+0     doi:10.1128/MCB.00095-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Liang, F., Jin, F., Liu, H., Wang, Y. (2009). The Molecular Function of the Yeast Polo-like Kinase Cdc5 in Cdc14 Release during Early Anaphase. Mol. Biol. Cell 20: 3671-3679 [Abstract] [Full Text]  
  • Diaz-Cuervo, H., Bueno, A. (2008). Cds1 Controls the Release of Cdc14-like Phosphatase Flp1 from the Nucleolus to Drive Full Activation of the Checkpoint Response to Replication Stress in Fission Yeast. Mol. Biol. Cell 19: 2488-2499 [Abstract] [Full Text]  
  • Schwartz, D. C., Felberbaum, R., Hochstrasser, M. (2007). The Ulp2 SUMO Protease Is Required for Cell Division following Termination of the DNA Damage Checkpoint. Mol. Cell. Biol. 27: 6948-6961 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»