Abstract
Candida albicans, a major opportunistic fungal pathogen of humans, can spontaneously undergo white-to-opaque switching, a prerequisite of mating. The phenotypes of white and opaque cells are heritable and bistable. The zinc-finger transcription factor Wor2 (White Opaque Regulator 2) has previously been identified as an important regulator of white-to-opaque switching. Deletion of WOR2 locks cells in the white phase when cultured on media containing glucose as the sole carbon source. In this study, we report that N-acetylglucosamine (GlcNAc) can induce white-to-opaque switching in the wor2/wor2 null mutant and stabilize the opaque phenotype of C. albicans. Moreover, overexpression of RAS1V13 (the activating form of RAS1) hypersensitizes white cells of the wor2/wor2 mutant to GlcNAc. These results suggest that Wor2 is not required for opaque cell formation at least under some culture conditions. Therefore C. albicans cells may adopt a different gene expression profile in response to GlcNAc to activate phenotypic switching.
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