Molecular Biology of the Cell Sign up for new MBC in Press e-TOCs!

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


     

MBC in Press, published online ahead of print April 23, 2008
Mol. Biol. Cell 10.1091/mbc.E08-02-0191

A more recent version of this article appeared on July 1, 2008
This Article
Right arrow Full Text (PDF)
Right arrow Supplemental Materials
Right arrow All Versions of this Article:
E08-02-0191v1
19/7/2741    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
Google Scholar
Right arrow Articles by Rauceo, J. M.
Right arrow Articles by Mitchell, A. P.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rauceo, J. M.
Right arrow Articles by Mitchell, A. P.

Submitted on February 21, 2008
Revised on April 7, 2008
Accepted on April 16, 2008

Regulation of the Candida albicans Cell Wall Damage Response by Transcription Factor Sko1 and PAS Kinase Psk1

Jason M. Rauceo,* Jill R. Blankenship,* Saranna Fanning,* Jessica J. Hamaker,* Jean-Sebastien Deneault,{dagger} Frank J. Smith,* Andre Nantel,{dagger} and Aaron P. Mitchell*

*Department of Microbiology and Institute of Cancer Research, Columbia University, New York, NY 10032; {dagger}Biotechology Research Institute, National Research Council of Canada, Montreal, Quebec H4P 2R2

Monitoring Editor: Kerry Bloom

The environmental niche of each fungus places distinct functional demands on the cell wall. Hence cell wall regulatory pathways may be highly divergent. We have pursued this hypothesis through analysis of C. albicans transcription factor mutants that are hypersensitive to caspofungin, an inhibitor of beta-1,3-glucan synthase. We report here that mutations in SKO1 cause this phenotype. C. albicans Sko1 undergoes Hog1-dependent phosphorylation after osmotic stress, like its S. cerevisiae ortholog, thus arguing that this Hog1-Sko1 relationship is conserved. However, Sko1 has a distinct role in the response to cell wall inhibition because: (1) sko1 mutants are much more sensitive to caspofungin than hog1 mutants; (2) Sko1 does not undergo detectable phosphorylation in response to caspofungin; (3) SKO1 transcript levels are induced by caspofungin in both wild-type and hog1 mutant strains; (4) sko1 mutants are defective in expression of caspofungin-inducible genes that are not induced by osmotic stress. Upstream Sko1 regulators were identified from a panel of caspofungin-hypersensitive protein kinase-defective mutants. Our results show that protein kinase Psk1 is required for expression of SKO1 and of Sko1-dependent genes in response to caspofungin. Thus Psk1 and Sko1 lie in a newly described signal transduction pathway.

Address correspondence to: Aaron P. Mitchell (apm4{at}columbia.edu)






Home Help [Feedback] [For Subscribers] [Archive] [Search] --
Copyright © 2008 by The American Society for Cell Biology. Terms of copyright protection, warranties, and disclaimers.