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Eukaryotic Cell, June 2004, p. 715-723, Vol. 3, No. 3
1535-9778/04/$08.00+0     DOI: 10.1128/EC.3.3.715-723.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Inducible Defense Mechanism against Nitric Oxide in Candida albicans{dagger}

Breanna D. Ullmann,1 Hadley Myers,1 Wiriya Chiranand,1 Anna L. Lazzell,2 Qiang Zhao,1 Luis A. Vega,1 Jose L. Lopez-Ribot,2 Paul R. Gardner,3 and Michael C. Gustin1*

Department of Biochemistry and Cell Biology, Rice University, Houston, Texas 77251-1892,1 Department of Medicine, Division of Infectious Diseases, The University of Texas Health Science Center at San Antonio, San Antonio, Texas 78245,2 Division of Critical Care Medicine, Children's Hospital Medical Center, Cincinnati, Ohio 452293

Received 27 August 2003/ Accepted 3 March 2004

The yeast Candida albicans is an opportunistic pathogen that threatens patients with compromised immune systems. Immune cell defenses against C. albicans are complex but typically involve the production of reactive oxygen species and nitrogen radicals such as nitric oxide (NO) that damage the yeast or inhibit its growth. Whether Candida defends itself against NO and the molecules responsible for this defense have yet to be determined. The defense against NO in various bacteria and the yeast Saccharomyces cerevisiae involves an NO-scavenging flavohemoglobin. The C. albicans genome contains three genes encoding flavohemoglobin-related proteins, CaYHB1, CaYHB4, and CaYHB5. To assess their roles in NO metabolism, we constructed strains lacking each of these genes and demonstrated that just one, CaYHB1, is responsible for NO consumption and detoxification. In C. albicans, NO metabolic activity and CaYHB1 mRNA levels are rapidly induced by NO and NO-generating agents. Loss of CaYHB1 increases the sensitivity of C. albicans to NO-mediated growth inhibition. In mice, infections with Candida strains lacking CaYHB1 still resulted in lethality, but virulence was decreased compared to that in wild-type strains. Thus, C. albicans possesses a rapid, specific, and highly inducible NO defense mechanism involving one of three putative flavohemoglobin genes.

* Corresponding author. Mailing address: Department of Biochemistry and Cell Biology, MS 140, Rice University, 6100 Main St., Houston, TX 77251-1892. Phone: (713) 348-5158. Fax: (713) 348-5154. E-mail: gustin{at}bioc.rice.edu.

{dagger} Supplemental material for this article may be found at http://ec.asm.org/.

Eukaryotic Cell, June 2004, p. 715-723, Vol. 3, No. 3
1535-9778/04/$08.00+0     DOI: 10.1128/EC.3.3.715-723.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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