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Originally published In Press as doi:10.1074/jbc.M209713200 on November 4, 2002

J. Biol. Chem., Vol. 278, Issue 3, 1713-1720, January 17, 2003
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Inactivation of Kex2p Diminishes the Virulence of Candida albicans*

George NewportDagger §, Alan KuoDagger §, Amy Flattery||, Charles Gill||, Julie J. BlakeDagger **, Myra B. Kurtz||, George K. Abruzzo||, and Nina AgabianDagger Dagger Dagger

From the Dagger  Department of Stomatology, University of California at San Francisco, California 94143-0422 and || Merck Research Laboratories, Rahway, New Jersey 07065-0900

Deletion of the kexin gene (KEX2) in Candida albicans has a pleiotropic effect on phenotype and virulence due partly to a defect in the expression of two major virulence factors: the secretion of active aspartyl proteinases and the formation of hyphae. kex2/kex2 mutants are highly attenuated in a mouse systemic infection model and persist within cultured macrophages for at least 24 h without causing damage. Pathology is modest, with little disruption of kidney matrix. The infecting mutant cells are largely confined to glomeruli, and are aberrant in morphology. The complex phenotype of the deletion mutants reflects a role for kexin in a wide range of cellular processes. Taking advantage of the specificity of Kex2p cleavage, an algorithm we developed to scan the 9168 open reading frames in Assembly 6 of the C. albicans genome identified 147 potential substrates of Kex2p. These include all previously identified substrates, including eight secreted aspartyl proteinases, the exoglucanase Xog1p, the immunodominant antigen Mp65, and the adhesin Hwp1p. Other putative Kex2p substrates identified include several adhesins, cell wall proteins, and hydrolases previously not implicated in pathogenesis. Kexins also process fungal mating pheromones; a modification of the algorithm identified a putative mating pheromone with structural similarities to Saccharomyces cerevisiae alpha -factor.

* This study was supported by National Institutes of Health Grants A133317, RO1DE12940, P01 DE07946-15S2, and PO1 DE07946.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ These authors contributed equally to this work.

Supported by University of California University-wide AIDS Research Program Grant F97-SF-048.

** Present address: Incyte Genomics, Palo Alto, CA 94304.

Dagger Dagger To whom correspondence should be addressed: Dept. of Stomatology, University of California, 521 Parnassus Avenue, Box 0422, San Francisco, CA 94243-0422. Tel.: 415-476-6845; Fax: 415-476-0664; Email: agabian@itsa.ucsf.edu.

Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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