N-acetylglucosamine-induced white-to-opaque switching in Candida albicans is independent of the Wor2 transcription factor

Fungal Genet Biol. 2014 Jan:62:71-7. doi: 10.1016/j.fgb.2013.10.005. Epub 2013 Oct 22.

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.

Keywords: Candida albicans; N-acetylglucosamine (GlcNAc); White-opaque switching; Wor2.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylglucosamine / metabolism*
  • Candida albicans / cytology
  • Candida albicans / physiology*
  • Fungal Proteins / physiology*
  • Gene Expression Regulation, Fungal
  • Genes, Mating Type, Fungal*
  • Mutation
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*

Substances

  • Fungal Proteins
  • Transcription Factors
  • Acetylglucosamine