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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.



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