ArticleNature genetics2013
Passage through the mammalian gut triggers a phenotypic switch that promotes Candida albicans commensalism.
Article in Nature genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 194 papers.
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Who cites it
194 citing papers in PubMed.
- The Mcu1 mitochondrial protein coordinates TCA cycle enzymes to modulate phenotypic switching and commensalism inVirulence · 2026Article
- The Gti1/Pac2 family protein CFG1 controls fungal chlamydospore formation through orchestrating cell wall remodeling, lipid metabolism, and ribosome biogenesis.Applied and environmental microbiology · 2026Article
- The unique Efg1 fungal virulence regulon in the catheterized bladder environment.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Invasive Candidiasis in Critically Ill Patients: Fundamental Concepts and Future Directions.Chest · 2026Review
- Population-scale chemical response revealed by a barcoded yeast collection.Nature communications · 2026Article
- Distinct properties of human pathogenicmSystems · 2026Article
- The hidden cost of antibiotics: microbial dysbiosis-induced SCFA imbalance and its underlying mechanisms.Frontiers in immunology · 2026Review
- Coordinated regulation of pH alkalinization by two transcription factors promotes fungal commensalism and pathogenicity.Nature communications · 2025Article
- Commensalism and pathogenesis of Candida albicans at the mucosal interface.Nature reviews. Microbiology · 2025Review
- Adaptive evolution ofmBio · 2025Article
- Exploring correlations between gut mycobiome and lymphocytes in melanoma patients undergoing anti-PD-1 therapy.Cancer immunology, immunotherapy : CII · 2025Article
- Image-based quantification of Candida albicans filamentation and hyphal length using the open-source visual programming language JIPipe.FEMS yeast research · 2025Article
- The impact of phenotypic heterogeneity on fungal pathogenicity and drug resistance.FEMS microbiology reviews · 2025Review
- Vaginal Candida albicans infections: host-pathogen-microbiome interactions.FEMS microbiology reviews · 2025Review
- Is Cryptococcus neoformans a pleomorphic fungus?Current opinion in microbiology · 2024Review
- Adaptation of Candida albicans to specific host environments by gain-of-function mutations in transcription factors.PLoS pathogens · 2024Review
- ControllingInfection and immunity · 2024Review
- The rod cell, a small form ofActa biochimica et biophysica Sinica · 2024Article
- Drivers of diversification in fungal pathogen populations.PLoS pathogens · 2024Review
- Review
134 more citing papers are in PubMed but not listed here.
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3 authors.
Funding
Abstract
Among ∼5,000,000 fungal species, C. albicans is exceptional in its lifelong association with humans, either within the gastrointestinal microbiome or as an invasive pathogen. Opportunistic infections are generally ascribed to defective host immunity but may require specific microbial programs. Here we report that exposure of C. albicans to the mammalian gut triggers a developmental switch, driven by the Wor1 transcription factor, to a commensal cell type. Wor1 expression was previously observed only in rare genetic backgrounds, where it controls a white-opaque switch in mating. We show that passage of wild-type cells through the mouse gastrointestinal tract triggers WOR1 expression and a novel phenotypic switch. The resulting GUT (gastrointestinally induced transition) cells differ morphologically and functionally from previously defined cell types, including opaque cells, and express a transcriptome that is optimized for the digestive tract. The white-GUT switch illuminates how a microorganism can use distinct genetic programs to transition between commensalism and invasive pathogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.