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MBC in Press, published online ahead of print July 19, 2005
Mol. Biol. Cell 10.1091/mbc.E05-05-0435

A more recent version of this article appeared on October 1, 2005
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Submitted on May 18, 2005
Revised on June 28, 2005
Accepted on July 13, 2005

Transcriptional Response of C. albicans to Nitric Oxide and the Role of the YHB1 Gene in Nitrosative Stress and Virulence

Bethann S. Hromatka, Suzanne M. Noble, and Alexander D. Johnson

Department of Microbiology and Immunology, University of California-San Francisco, San Francisco, CA 94143

Monitoring Editor: Mark Solomon

Here, we investigate how Candida albicans, the most prevalent human fungal pathogen, protects itself from nitric oxide (NO·), an antimicrobial compound produced by the innate immune system. We show that exposure of C. albicans to NO· elicits a reproducible and specific transcriptional response as determined by genome-wide microarray analysis. Many genes are transiently induced or repressed by NO·, whereas a set of nine genes remain at elevated levels during NO· exposure. The most highly induced gene in this latter category is YHB1, a flavohemoglobin that detoxifies NO· in C. albicans and other microbes. We show that C. albicans strains deleted for YHB1 have two phenotypes in vitro; they are hypersensitive to NO· and they are hyperfilamentous. In a mouse model of disseminated candidiasis, a YHB1 deleted C. albicans strain shows moderately attenuated virulence, but the virulence defect is not suppressed by deletion of the host NOS2 gene. These results suggest that NO· production is not a prime determinant of virulence in the mouse tail vein model of candidiasis and that the attenuated virulence of a yhb1{Delta}/yhb1{Delta} strain is attributable to a defect other than its reduced ability to detoxify NO·.

Address correspondence to: Alexander D. Johnson (ajohnson{at}cgl.ucsf.edu)




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