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Abstract

Candida albicans is an opportunistic fungal pathogen that is found in the normal gastrointestinal flora of most healthy humans. However, in immunocompromised patients, blood-stream infections often cause death, despite the use of anti-fungal therapies. The recent completion of the C. albicans genome sequence, the availability of whole-genome microarrays and the development of tools for rapid molecular-genetic manipulations of the C. albicans genome are generating an explosion of information about the intriguing biology of this pathogen and about its mechanisms of virulence. They also reveal the extent of similarities and differences between C. albicans and its benign relative, Saccharomyces cerevisiae.

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Nonfilamentous C. albicans mutants are avirulent.

Hsiu-Jung Lo, Julia Köhler, Beth DiDomenico … (1997)

Candida albicans and Saccharomyces cerevisiae switch from a yeast to a filamentous form. In Saccharomyces, this switch is controlled by two regulatory proteins, Ste12p and Phd1p. Single-mutant strains, ste12/ste12 or phd1/phd1, are partially defective, whereas the ste12/ste12 phd1/phd1 double mutant is completely defective in filamentous growth and is noninvasive. The equivalent cph1/cph1 efg1/efg1 double mutant in Candida (Cph1p is the Ste12p homolog and Efg1p is the Phd1p homolog) is also defective in filamentous growth, unable to form hyphae or pseudohyphae in response to many stimuli, including serum or macrophages. This Candida cph1/cph1 efg1/efg1 double mutant, locked in the yeast form, is avirulent in a mouse model.

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Suppression of hyphal formation in Candida albicans by mutation of a STE12 homolog.

H. Liu, J. Kohler, G. R. Fink (1994)

A Candida albicans gene (CPH1) was cloned that encodes a protein homologous to Saccharomyces cerevisiae Ste12p, a transcription factor that is the target of the pheromone response mitogen-activated protein kinase cascade. CPH1 complements both the mating defect of ste12 haploids and the filamentous growth defect of ste12/ste12 diploids. Candida albicans strains without a functional CPH1 gene (cph1/cph1) show suppressed hyphal formation on solid medium. However, cph1/cph1 strains can still form hyphae in liquid culture and in response to serum. Thus, filamentous growth may be activated in C. albicans by the same signaling kinase cascade that activates Ste12p in S. cerevisiae; however, alternative pathways may exist in C. albicans.

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White-opaque switching in Candida albicans is controlled by mating-type locus homeodomain proteins and allows efficient mating.

Daniel G. Miller, Matthew D. Johnson (2002)

Discovered over a decade ago, white-opaque switching in the human fungal pathogen Candida albicans is an alternation between two quasistable, heritable transcriptional states. Here, we show that white-opaque switching and sexual mating are both controlled by mating type locus homeodomain proteins and that opaque cells mate approximately 10(6) times more efficiently than do white cells. These results show that opaque cells are a mating-competent form of C. albicans and that this pathogen undergoes a white-to-opaque switch as a critical step in the mating process. As white cells are generally more robust in a mammalian host than are opaque cells, this strategy allows the organism to survive the rigors of life within a mammalian host, yet generate mating-competent cells.

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DOI:: 10.1038/nrg948

PubMed ID:: 12459722

ScienceOpen disciplines: Chemistry

Keywords: Morphogenesis,pathogenicity,Transcription, Genetic,Candida albicans,Genome, Fungal,Saccharomyces cerevisiae,Mutagenesis,Gene Deletion,genetics,Phenotype,Transfection,physiology,Signal Transduction

Candida Albicans: a molecular revolution built on lessons from budding yeast.

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Most cited references 85

Nonfilamentous C. albicans mutants are avirulent.

Suppression of hyphal formation in Candida albicans by mutation of a STE12 homolog.

White-opaque switching in Candida albicans is controlled by mating-type locus homeodomain proteins and allows efficient mating.

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