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 Nicholls, S.
Right arrow Articles by Brown, A. J. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nicholls, S.
Right arrow Articles by Brown, A. J. P.

 Previous Article  |  Next Article 

Eukaryotic Cell, October 2004, p. 1111-1123, Vol. 3, No. 5
1535-9778/04/$08.00+0     DOI: 10.1128/EC.3.5.1111-1123.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Msn2- and Msn4-Like Transcription Factors Play No Obvious Roles in the Stress Responses of the Fungal Pathogen Candida albicans{dagger}

Susan Nicholls,1 Melissa Straffon,1,{ddagger} Brice Enjalbert,2 André Nantel,2 Susan Macaskill,1 Malcolm Whiteway,2 and Alistair J. P. Brown1*

Molecular and Cell Biology, Institute of Medical Sciences, University of Aberdeen, Aberdeen, United Kingdom,1 Eukaryotic Genetics Group, NRC Biotechnology Research Institute, Montreal, Quebec, Canada2

Received 10 January 2004/ Accepted 7 June 2004

In Saccharomyces cerevisiae, the (C2H2)2 zinc finger transcription factors Msn2 and Msn4 play central roles in responses to a range of stresses by activating gene transcription via the stress response element (STRE; CCCCT). The pathogen Candida albicans displays stress responses that are thought to help it survive adverse environmental conditions encountered within its human host. However, these responses differ from those in S. cerevisiae, and hence we predicted that the roles of Msn2- and Msn4-like proteins might have been functionally reassigned in C. albicans. C. albicans has two such proteins: CaMsn4 and Mnl1 (for Msn2- and Msn4-like). CaMSN4, but not MNL1, weakly complemented the inability of an S. cerevisiae msn2 msn4 mutant to activate a STRE-lacZ reporter. Also, the disruption of CaMsn4 and Mnl1 had no discernible effect upon the resistance of C. albicans to heat, osmotic, ethanol, nutrient, oxidative, or heavy-metal stress or upon the stress-activated transcriptome in C. albicans. Furthermore, although Cap1-dependent activation of a Yap response element-luciferase reporter was observed, a STRE reporter was not activated in response to stresses in C. albicans. Ectopic expression of CaMsn4 or Mnl1 did not affect the cellular or molecular responses of C. albicans to stress. Under the conditions tested, the putative activation and DNA binding domains of CaMsn4 did not appear to be functional. These data suggest that CaMsn4 and Mnl1 do not contribute significantly to stress responses in C. albicans. The data are consistent with the idea that stress signaling in this fungus has diverged significantly from that in budding yeast.

* Corresponding author. Mailing address: Aberdeen Fungal Group, Institute of Medical Sciences, University of Aberdeen, Aberdeen AB25 2ZD, United Kingdom. Phone: 44-1224-555883. Fax: 44-1224-555844. E-mail: Al.Brown{at}abdn.ac.uk.

{dagger} This is NRC publication no. 46183.

{ddagger} Present address: CSIRO Molecular Science, Clayton South, Victoria 3169, Australia.

Eukaryotic Cell, October 2004, p. 1111-1123, Vol. 3, No. 5
1535-9778/04/$08.00+0     DOI: 10.1128/EC.3.5.1111-1123.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Sellam, A., Askew, C., Epp, E., Lavoie, H., Whiteway, M., Nantel, A. (2009). Genome-wide Mapping of the Coactivator Ada2p Yields Insight into the Functional Roles of SAGA/ADA Complex in Candida albicans. Mol. Biol. Cell 20: 2389-2400 [Abstract] [Full Text]  
  • Bahn, Y.-S. (2008). Master and Commander in Fungal Pathogens: the Two-Component System and the HOG Signaling Pathway. Eukaryot Cell 7: 2017-2036 [Full Text]  
  • Cuellar-Cruz, M., Briones-Martin-del-Campo, M., Canas-Villamar, I., Montalvo-Arredondo, J., Riego-Ruiz, L., Castano, I., De Las Penas, A. (2008). High Resistance to Oxidative Stress in the Fungal Pathogen Candida glabrata Is Mediated by a Single Catalase, Cta1p, and Is Controlled by the Transcription Factors Yap1p, Skn7p, Msn2p, and Msn4p. Eukaryot Cell 7: 814-825 [Abstract] [Full Text]  
  • Bahn, Y.-S., Molenda, M., Staab, J. F., Lyman, C. A., Gordon, L. J., Sundstrom, P. (2007). Genome-Wide Transcriptional Profiling of the Cyclic AMP-Dependent Signaling Pathway during Morphogenic Transitions of Candida albicans. Eukaryot Cell 6: 2376-2390 [Abstract] [Full Text]  
  • Argimon, S., Wishart, J. A., Leng, R., Macaskill, S., Mavor, A., Alexandris, T., Nicholls, S., Knight, A. W., Enjalbert, B., Walmsley, R., Odds, F. C., Gow, N. A. R., Brown, A. J. P. (2007). Developmental Regulation of an Adhesin Gene during Cellular Morphogenesis in the Fungal Pathogen Candida albicans. Eukaryot Cell 6: 682-692 [Abstract] [Full Text]  
  • Martchenko, M., Levitin, A., Whiteway, M. (2007). Transcriptional Activation Domains of the Candida albicans Gcn4p and Gal4p Homologs. Eukaryot Cell 6: 291-301 [Abstract] [Full Text]  
  • Hernandez-Lopez, M. J., Randez-Gil, F., Prieto, J. A. (2006). Hog1 Mitogen-Activated Protein Kinase Plays Conserved and Distinct Roles in the Osmotolerant Yeast Torulaspora delbrueckii.. Eukaryot Cell 5: 1410-1419 [Abstract] [Full Text]  
  • Tournu, H., Tripathi, G., Bertram, G., Macaskill, S., Mavor, A., Walker, L., Odds, F. C., Gow, N. A. R., Brown, A. J. P. (2005). Global Role of the Protein Kinase Gcn2 in the Human Pathogen Candida albicans. Eukaryot Cell 4: 1687-1696 [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»