Journal
MOLECULAR BIOLOGY OF THE CELL
Volume 16, Issue 10, Pages 4814-4826Publisher
AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E05-05-0435
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- NIAID NIH HHS [R01 AI049187, R01 AI49187] Funding Source: Medline
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Here, we investigate how Candida albicans, the most prevalent human fungal pathogen, protects itself from nitric oxide ((NO)-N-center dot), an antimicrobial compound produced by the innate immune system. We show that exposure of C. albicans to (NO)-N-center dot elicits a reproducible and specific transcriptional response as determined by genome-wide microarray analysis. Many genes are transiently induced or repressed by (NO)-N-center dot, whereas a set of nine genes remain at elevated levels during (NO)-N-center dot exposure. The most highly induced gene in this latter category is YHB1, a flavohemoglobin that detoxifies (NO)-N-center dot 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)-N-center dot 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)-N-center dot 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)-N-center dot.
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