| First Author | Hromatka BS | Year | 2005 |
| Journal | Mol Biol Cell | Volume | 16 |
| Issue | 10 | Pages | 4814-26 |
| PubMed ID | 16030247 | Mgi Jnum | J:106530 |
| Mgi Id | MGI:3618939 | Doi | 10.1091/mbc.E05-05-0435 |
| Citation | Hromatka BS, et al. (2005) Transcriptional response of Candida albicans to nitric oxide and the role of the YHB1 gene in nitrosative stress and virulence. Mol Biol Cell 16(10):4814-26 |
| abstractText | 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 yhb1delta/yhb1delta strain is attributable to a defect other than its reduced ability to detoxify *NO. |
