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Vol. 17, Issue 2, 1018-1032, February 2006

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Role of the Hog1 Stress-activated Protein Kinase in the Global Transcriptional Response to Stress in the Fungal Pathogen Candida albicans

Brice Enjalbert ^* , Deborah A. Smith  , Michael J. Cornell , Intikhab Alam , Susan Nicholls ^* ||, Alistair J.P. Brown ^*, and Janet Quinn 

^* Aberdeen Fungal Group, School of Medical Sciences, Institute of Medical Sciences, University of Aberdeen, Aberdeen AB25 2ZD, United Kingdom; Institute of Cell and Molecular Biosciences, University of Newcastle upon Tyne, Newcastle upon Tyne NE2 4HH, United Kingdom; and School of Computer Science, University of Manchester, Manchester M13 9PL, United Kingdom

Submitted June 7, 2005; Revised November 2, 2005; Accepted November 30, 2005
Monitoring Editor: Susan Wente

The resistance of Candida albicans to many stresses is dependent on the stress-activated protein kinase (SAPK) Hog1. Hence we have explored the role of Hog1 in the regulation of transcriptional responses to stress. DNA microarrays were used to characterize the global transcriptional responses of HOG1 and hog1 cells to three stress conditions that activate the Hog1 SAPK: osmotic stress, oxidative stress, and heavy metal stress. This revealed both stress-specific transcriptional responses and a core transcriptional response to stress in C. albicans. The core transcriptional response was characterized by a subset of genes that responded in a stereotypical manner to all of the stresses analyzed. Inactivation of HOG1 significantly attenuated transcriptional responses to osmotic and heavy metal stresses, but not to oxidative stress, and this was reflected in the role of Hog1 in the regulation of C. albicans core stress genes. Instead, the Cap1 transcription factor plays a key role in the oxidative stress regulation of C. albicans core stress genes. Our data show that the SAPK network in C. albicans has diverged from corresponding networks in model yeasts and that the C. albicans SAPK pathway functions in parallel with other pathways to regulate the core transcriptional response to stress.

The online version of this article contains supplemental material at MBC Online (http://www.molbiolcell.org).

These authors contributed equally to this work.

^|| Present address: Department of Molecular and Cellular Pharmacology, 1580 NW 10th Avenue, University of Miami, FL 33136.

Address correspondence to: Janet Quinn (janet.quinn{at}ncl.ac.uk) or Alistair J.P. Brown (Al.Brown{at}abdn.ac.uk).

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