ArticlePLoS biology2013
Candida albicans commensalism and pathogenicity are intertwined traits directed by a tightly knit transcriptional regulatory circuit.
Article in PLoS biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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Who cites it
98 citing papers in PubMed, 158 citations in OpenAlex.
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- Adaptation of Candida albicans to specific host environments by gain-of-function mutations in transcription factors.PLoS pathogens · 2024Review
- Temporal transcriptional response ofeLife · 2024Article
- Functional genomic analysis of genes important for Candida albicans fitness in diverse environmental conditions.Cell reports · 2024Article
- Systematic analysis of themBio · 2024Article
- RFX transcription factor in the human-associated yeast Candida albicans regulates adhesion to oral epithelium.Molecular microbiology · 2024Article
- Sinefungin, a natural nucleoside analog of S-adenosyl methionine, impairs the pathogenicity ofnpj antimicrobials and resistance · 2024Article
- Inflammatory cytokine signalling in vulvovaginal candidiasis: a hot mess driving immunopathology.Oxford open immunology · 2024Review
- Commensal fungi in intestinal health and disease.Nature reviews. Gastroenterology & hepatology · 2023Review
- Sinefungin, a natural nucleoside analog of S-adenosyl methionine, impairs the pathogenicity ofbioRxiv : the preprint server for biology · 2023Article
- Host-derived reactive oxygen species trigger activation of the Candida albicans transcription regulator Rtg1/3.PLoS pathogens · 2023Article
- Multifactor transcriptional control of alternative oxidase induction integrates diverse environmental inputs to enable fungal virulence.Nature communications · 2023Article
- Analysis of Pneumocystis Transcription Factor Evolution and Implications for Biology and Lifestyle.mBio · 2023Article
38 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Systemic, life-threatening infections in humans are often caused by bacterial or fungal species that normally inhabit a different locale in our body, particularly mucosal surfaces. A hallmark of these opportunistic pathogens, therefore, is their ability to thrive in disparate niches within the host. In this work, we investigate the transcriptional circuitry and gene repertoire that enable the human opportunistic fungal pathogen Candida albicans to proliferate in two different niches. By screening a library of transcription regulator deletion strains in mouse models of intestinal colonization and systemic infection, we identified eight transcription regulators that play roles in at least one of these models. Using genome-wide chromatin immunoprecipitation, we uncovered a network comprising ∼800 target genes and a tightly knit transcriptional regulatory circuit at its core. The network is enriched with genes upregulated in C. albicans cells growing in the host. Our findings indicate that many aspects of commensalism and pathogenicity are intertwined and that the ability of this microorganism to colonize multiple niches relies on a large, integrated circuit.
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Registered trials
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.