Candida albicans commensalism and pathogenicity are intertwined traits directed by a tightly knit transcriptional regulatory circuit
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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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Earlier work in respiratory competent C. albicans indicated that the Rtg pathway is involved in processes related to infectivity, filamentous growth and niche adaptation, crucial for the commensal/opportunistic pathogen lifestyle of this yeast species.
“Earlier work performed in respiratory competent C. albicans indicated that the Rtg pathway is involved in the processes related to infectivity, filamentous growth and niche adaptation, crucial for the commensal/opportunistic pathogen lifestyle of this yeast species (Pérez et al. 2013; Yan et al. 2014).”
From Mitochondrial retrograde control of transcription evolves with respiratory stress, metabolic adaptation, and virulence in budding yeasts (2026) · cites this paper as Pérez et al. 2013
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Experimental — accuracy not yet measuredThis function is important for infectivity, pathogenicity, and survival within the animal host of C. albicans.
“This function is important for infectivity, pathogenicity, and survival within the animal host of this yeast species”
From Mitochondrial retrograde control of transcription evolves with respiratory stress, metabolic adaptation, and virulence in budding yeasts (2026) · cites this paper as Pérez et al. 2013
CaRtg1 and CaRtg3 are involved in sphingolipid homeostasis and adaptation to commensalism and pathogenicity.
“CaRtg1 and CaRtg3 were also shown to be involved in sphingolipid homeostasis (Moreno-Velásquez et al. 2020), and adaptation to commensalism and pathogenicity (Pérez et al. 2013).”
From Mitochondrial retrograde control of transcription evolves with respiratory stress, metabolic adaptation, and virulence in budding yeasts (2026) · cites this paper as Pérez et al. 2013
Rtg transcription factors, together with Hms1 and Tye7, were shown to be a key part of a regulatory circuit controlling diverse metabolic processes related to commensalism and pathogenicity, as well as sphingolipid homeostasis.
“Together with several other transcription factors, such as Hms1 and Tye7, they were shown to be a key part of a regulatory circuit that controls diverse metabolic processes related to multiple aspects of commensalism and pathogenicity (Pérez et al. 2013), as well as the sphingolipid homeostasis (Moreno-Velásquez et al. 2020).”
From Mitochondrial retrograde control of transcription evolves with respiratory stress, metabolic adaptation, and virulence in budding yeasts (2026) · cites this paper as Pérez et al. 2013
A genome-wide chromatin immunoprecipitation study previously reported that C. albicans Rtg1 and Rtg3 share the same consensus binding sequence.
“A genome-wide chromatin immunoprecipitation (ChIP) study previously reported that C. albicans Rtg1 and Rtg3 share the same consensus binding sequence34.”
From Multifactor transcriptional control of alternative oxidase induction integrates diverse environmental inputs to enable fungal virulence (2023) · cites this paper as [34]
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References 60 · Cited by 156
Research works printed but not linked: 2
- [10]Calderone RA, Gow NA (2002) Host recognition by Candida species. Calderone RA, editor. Candida and Candidiasis. Washington (D.C.): ASM Press. pp. 67–86.
- [11]Hube B, Naglik JR (2002) Extracellular Hydrolases. Calderone RA, editor. Candida and Candidiasis. Washington (D.C.): ASM Press. pp. 107–122.
- Authors
- Pérez, J. C., Kumamoto, C. A., & Johnson, A. D.
- Affiliations
- University of California, San Francisco (US)
- Tufts University (US)
- Corresponding author
- Pérez, J. Christian
- Venue
- PLoS Biology
- Publisher
- Public Library of Science (PLoS)
- Published
- 2013-03-19
- Volume
- 11
- Issue
- 3
- Pages
- e1001510
- ISSN
- 1544-9173 (ISSN-L)
- 1545-7885
- PMC
- PMC3601966
- OpenAlex
- W2020653359
- Cited by
- 156
- References
- 60
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 12 · 2023: 7 · 2022: 10 · 2021: 15 · 2020: 19 · 2019: 14 · 2018: 13 · 2017: 9 · 2016: 9 · 2015: 18 · 2014: 15 · 2013: 7
- FWCI
- 7.31
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS Biology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Funders
- American Heart Association
- University of California, San Francisco
- National Institute of Allergy and Infectious Diseases (R01AI049187, R01AI081794, AI081794)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Health Sciences › Medicine › Epidemiology › Fungal Infections and Studies
- Keywords
- Candida albicans, commensalism, pathogenicity, transcriptional regulatory networks, transcription factors, intestinal colonization, systemic infection, opportunistic fungal pathogens, chromatin immunoprecipitation, transcription factor target genes, gene deletion screen
- MeSH terms
- Animals, Candida albicans, Candidiasis, Female, Fungal Proteins, Humans, Mice, Inbred BALB C, Transcription Factors, Gene Expression Regulation, Fungal, Mice
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