ArticlePLoS pathogens2013
Activation of the Cph1-dependent MAP kinase signaling pathway induces white-opaque switching in Candida albicans.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Transcriptomic meta-analysis to identify potential antifungal targets in Candida albicans.BMC microbiology · 2024Pooled it
- Molecular mechanisms, pathogenesis and therapeutic advances ofFrontiers in cellular and infection microbiology · 2026Review
- Genetic and environmental control of parasexual reproduction in the pathogenicMicrobiology and molecular biology reviews : MMBR · 2025Review
- Transcriptional control ofmBio · 2025Article
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- The Ypk1 protein kinase signaling pathway is rewired and not essential for viability in Candida albicans.PLoS genetics · 2023Article
- Functional genomic analysis ofiScience · 2023Article
- Farnesol and phosphorylation of the transcriptional regulator Efg1 affect Candida albicans white-opaque switching rates.PloS one · 2023Article
- Mucosal Infection with Unmasked Candida albicans Cells Impacts Disease Progression in a Host Niche-Specific Manner.Infection and immunity · 2022Article
- Functional analysis of theiScience · 2022Article
- Overexpression approaches to advance understanding of Candida albicans.Molecular microbiology · 2022Review
- When Is It Appropriate to Take Off the Mask? Signaling Pathways That Regulate ß(1,3)-Glucan Exposure inFrontiers in fungal biology · 2022Article
- The protein kinase Ire1 has a Hac1-independent essential role in iron uptake and virulence of Candida albicans.PLoS pathogens · 2022Article
- A Suppressor Mutation in the β-Subunit Kis1 Restores Functionality of the SNF1 Complex inmSphere · 2021Article
- Fungal Cell Wall Proteins and Signaling Pathways Form a Cytoprotective Network to Combat Stresses.Journal of fungi (Basel, Switzerland) · 2021Review
- Activation of Cph1 causes ß(1,3)-glucan unmasking in Candida albicans and attenuates virulence in mice in a neutrophil-dependent manner.PLoS pathogens · 2021Article
- Advances in fungal chemical genomics for the discovery of new antifungal agents.Annals of the New York Academy of Sciences · 2021Review
- Underlying mechanisms of the effect of minocycline againstExperimental and therapeutic medicine · 2021Article
- Signal-mediated localization of Candida albicans pheromone response pathway components.G3 (Bethesda, Md.) · 2021Article
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Depending on the environmental conditions, the pathogenic yeast Candida albicans can undergo different developmental programs, which are controlled by dedicated transcription factors and upstream signaling pathways. C. albicans strains that are homozygous at the mating type locus can switch from the normal yeast form (white) to an elongated cell type (opaque), which is the mating-competent form of this fungus. Both white and opaque cells use the Ste11-Hst7-Cek1/Cek2 MAP kinase signaling pathway to react to the presence of mating pheromone. However, while opaque cells employ the transcription factor Cph1 to induce the mating response, white cells recruit a different downstream transcription factor, Tec1, to promote the formation of a biofilm that facilitates mating of opaque cells in the population. The switch from the white to the opaque cell form is itself induced by environmental signals that result in the upregulation of the transcription factor Wor1, the master regulator of white-opaque switching. To get insight into the upstream signaling pathways controlling the switch, we expressed all C. albicans protein kinases from a tetracycline-inducible promoter in a switching-competent strain. Screening of this library of strains showed that a hyperactive form of Ste11 lacking its N-terminal domain (Ste11(ΔN467)) efficiently stimulated white cells to switch to the opaque phase, a behavior that did not occur in response to pheromone. Ste11(ΔN467)-induced switching specifically required the downstream MAP kinase Cek1 and its target transcription factor Cph1, but not Cek2 and Tec1, and forced expression of Cph1 also promoted white-opaque switching in a Wor1-dependent manner. Therefore, depending on the activation mechanism, components of the pheromone-responsive MAP kinase pathway can be reconnected to stimulate an alternative developmental program, switching of white cells to the mating-competent opaque phase.
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