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Eukaryotic Cell, June 2004, p. 764-775, Vol. 3, No. 3
1535-9778/04/$08.00+0     DOI: 10.1128/EC.3.3.764-775.2004

Hemoglobin Regulates Expression of an Activator of Mating-Type Locus {alpha} Genes in Candida albicans

Michael L. Pendrak, S. Steve Yan,{dagger} and David D. Roberts*

Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-1500

Received 8 September 2003/ Accepted 24 March 2004

Phenotypic switching from the white to the opaque phase is a necessary step for mating in the pathogenic fungus Candida albicans. Suppressing switching during vascular dissemination of the organism may be advantageous, because opaque cells are more susceptible to host defenses. A repressor of white-opaque switching, HBR1 (hemoglobin response gene 1), was identified based on its specific induction following growth in the presence of exogenous hemoglobin. Deletion of a single HBR1 allele allowed opaque phase switching and mating competence, accompanied by a lack of detectable MTL {alpha}1 and {alpha}2 gene expression and enhanced MTLa1 gene expression. Conversely, overexpression of Hbr1p or exposure to hemoglobin increased MTL{alpha} gene expression. The a1/{alpha}2 repressed target gene CAG1 was derepressed in the same mutant in a hemoglobin-sensitive manner. Regulation of CAG1 by hemoglobin required an intact MTLa1 gene. Several additional Mtlp targets were perturbed in HBR1 mutants in a manner consistent with commitment to an a mating phenotype, including YEL007w, MF{alpha}, HST6, and RAM2. Therefore, Hbr1 is part of a host factor-regulated signaling pathway that controls white-opaque switching and mating in the absence of allelic deletion at the MTL locus.

* Corresponding author. Mailing address: National Cancer Institute, 10 Center Dr., MSC 1500, Building 10, Room 2A33, Bethesda, MD 20892. Phone: (301) 496-6264. Fax: (301) 402-0043. E-mail: droberts{at}helix.nih.gov.

{dagger} Present address: FDA, Rockville, MD 20855.

Eukaryotic Cell, June 2004, p. 764-775, Vol. 3, No. 3
1535-9778/04/$08.00+0     DOI: 10.1128/EC.3.3.764-775.2004




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