Molecular Biology of the Cell Call for Nominations: MBC Editor-in-Chief

Home Help [Feedback] [For Subscribers] [Archive] [Search] --
QUICK SEARCH:   [advanced]


     

MBC in Press, published online ahead of print December 20, 2006
Mol. Biol. Cell 10.1091/mbc.E06-05-0442

A more recent version of this article appeared on March 1, 2007
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
E06-05-0442v1
18/3/815    most recent
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 arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Shi, Q.-M.
Right arrow Articles by Wang, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Shi, Q.-M.
Right arrow Articles by Wang, Y.

Submitted on May 22, 2006
Revised on November 27, 2006
Accepted on December 4, 2006

Critical Role of DNA Checkpoints in Mediating Genotoxic-Stress-induced Filamentous Growth in Candida albicans

Qing-Mei Shi, Yan-Ming Wang, Xin-De Zheng, Raymond Teck Ho Lee, and Yue Wang

Institute of Molecular and Cell Biology, ASTAR Biological Sciences Institutes, Singapore 138673

Monitoring Editor: John Pringle

The polymorphic fungus C. albicans switches from yeast to filamentous growth in response to a range of genotoxic insults, including inhibition of DNA synthesis by hydroxyurea (HU) or aphidicolin (AC), depletion of the ribonucleotide-reductase subunit Rnr2p, and DNA damage induced by methylmethane sulfonate (MMS) or UV light (UV). Deleting RAD53, which encodes a downstream effector kinase for both the DNA-replication and DNA-damage checkpoint pathways, completely abolished the filamentous growth caused by all the genotoxins tested. Deleting RAD9, which encodes a signal transducer of the DNA-damage checkpoint, specifically blocked the filamentous growth induced by MMS or UV but not that induced by HU or AC. Deleting MRC1, the counterpart of RAD9 in the DNA-replication checkpoint, impaired DNA synthesis and caused cell elongation even in the absence of external genotoxic insults. Together, the results indicate that the DNA-replication/damage checkpoints are critically required for the induction of filamentous growth by genotoxic stress. In addition, either of two mutations in the FHA1 domain of Rad53p, G65A and N104A, nearly completely blocked the filamentous-growth response but had no significant deleterious effect on cell-cycle arrest. These results suggest that the FHA domain, known for its ability to bind phosphopeptides, has an important role in mediating genotoxic-stress-induced filamentous growth and that such growth is a specific, Rad53p-regulated cellular response in C. albicans.

Address correspondence to: Yue Wang (mcbwangy{at}imcb.a-star.edu.sg)




This article has been cited by other articles:


Home page
 J. Cell Sci.Home page
K. R. Finley, K. J. Bouchonville, A. Quick, and J. Berman
Dynein-dependent nuclear dynamics affect morphogenesis in Candida albicans by means of the Bub2p spindle checkpoint
J. Cell Sci., February 15, 2008; 121(4): 466 - 476.
[Abstract] [Full Text] [PDF]

Home page
 GeneticsHome page
I. Malavazi, J. F. Lima, P. A. de Castro, M. Savoldi, M. H. de Souza Goldman, and G. H. Goldman
Genetic Interactions of the Aspergillus nidulans atmAATM Homolog With Different Components of the DNA Damage Response Pathway
Genetics, February 1, 2008; 178(2): 675 - 691.
[Abstract] [Full Text] [PDF]

Home page
 Eukaryot CellHome page
M. Legrand, C. L. Chan, P. A. Jauert, and D. T. Kirkpatrick
Role of DNA Mismatch Repair and Double-Strand Break Repair in Genome Stability and Antifungal Drug Resistance in Candida albicans
Eukaryot. Cell, December 1, 2007; 6(12): 2194 - 2205.
[Abstract] [Full Text] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] --
Copyright © 2006 by The American Society for Cell Biology. Terms of copyright protection, warranties, and disclaimers.