The calcineurin pathway regulates extreme thermotolerance, cell membrane and wall integrity, antifungal resistance, and virulence in Candida auris
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Abstract
Candida auris, an emerging fungal pathogen characterized by its multidrug resistance and high mortality rates, poses a significant public health challenge. Despite its importance, the signaling pathways governing virulence and antifungal resistance in C. auris remain poorly understood. This study investigates the calcineurin pathway in C. auris, critical for virulence and antifungal resistance in other fungal pathogens. Calcineurin, a calcium/calmodulin-dependent protein phosphatase, comprises a catalytic subunit (Cna1) and a regulatory subunit (Cnb1) in C. auris. Our findings reveal that deletion of CNA1 or CNB1 disrupts extreme thermotolerance and cell membrane and wall integrity, leading to increased susceptibility to azoles and echinocandins. Moreover, we identified a downstream transcription factor, Crz1, which plays a central role in this pathway in other fungal species. Deletion of CRZ1 resulted in thermotolerance and membrane integrity defects comparable to those of cna1Δ and cnb1Δ mutants, along with increased azole susceptibility. Supporting it, fluconazole treatment induced Crz1 nuclear translocation in a Cna1-dependent manner. However, unlike cna1Δ and cnb1Δ mutants, the crz1Δ mutant displayed increased resistance to echinocandins, suggesting the opposing roles for Crz1 in regulating cell wall integrity. Nevertheless, echinocandins also promoted Crz1 nuclear translocation via Cna1, underscoring the complex regulatory mechanisms at play. Cna1 was found to be required for virulence in both the Drosophila systemic infection model and the murine skin infection model. However, in a systemic murine infection model, both calcineurin and Crz1 appeared dispensable for C. auris virulence. Our findings highlight that the evolutionarily conserved calcineurin pathway employs distinct regulatory mechanisms to perform divergent roles in regulating extreme thermotolerance, cell wall and membrane integrity, antifungal drug resistance, and virulence in C. auris.
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The role of calcineurin in drug tolerance, persistence, and stable resistance is documented.
“While its role in drug tolerance, persistence, and stable resistance is documented [19, 20, 21, 22]”
From Calcineurin‐Dependent Stress Adaptation Enables Caspofungin Heteroresistance Leading to Stable Resistance in <i>Candida Glabrata</i> (2026) · cites this paper as [19]
The Results section, “Calcineurin promotes tolerance to azoles and echinocandins in C. auris” (page unavailable), supports a role for calcineurin in drug tolerance; the Discussion also reports changes in antifungal resistance. Our copy does not establish a role in drug persistence or specifically in stable resistance. (LLM, conf=0.84)
Experimental — accuracy not yet measuredC. auris regulates other stress resistance pathways, such as calcineurin and Ras/cAMP/PKA pathways for thermotolerance, morphological plasticity, and biofilm formation, which contribute to pathogenesis in C. auris.
“C. auris further regulates other stress resistance pathways, such as calcineurin [78] and Ras/cAMP/PKA [79] pathways for thermotolerance, morphological plasticity, and biofilm formation, which contribute to pathogenesis in C. auris.”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [78]
The Discussion (page not provided) supports a role for calcineurin in extreme thermotolerance and pathogenicity in C. auris. But the Results section explicitly finds that calcineurin does not regulate pseudohyphal formation or biofilm formation, contrary to those parts of the claim. The separate Ras/cAMP/PKA citation is not assessed here. (LLM, conf=0.90)
Experimental — accuracy not yet measuredCNA1 is indispensable for virulence properties needed for C. auris skin colonization and infection.
“This suggests that the CNA1 is indispensable for virulence properties needed for C. auris skin colonization and infection [78].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [78]
Ablation of the calcineurin pathway by CNA1 deletion in C. auris significantly reduced abscess and fungal burden in the murine skin in a subcutaneous infection model.
“Cha and colleagues demonstrated that ablation of the calcineurin pathway by CNA1 deletion in C. auris significantly reduced abscess and fungal burden in the murine skin in a subcutaneous infection model [78].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [78]
In ex vivo murine skin, the Δcna1 strain had significantly lower adhesion to the skin shortly post-association.
“In ex vivo murine skin, the Δcna1 strain had significantly lower adhesion to the skin shortly post-association [78].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [78]
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- Authors
- Cha, H., Won, D., Kang, S., Kim, E.-S., Lee, K.-A., Lee, W.-J., Lee, K.-T., & Bahn, Y.-S.
- Affiliations
- Yonsei University (KR)
- Jeonbuk National University (KR)
- Seoul National University (KR)
- Corresponding author
- Bahn, Yong-Sun
- ORCID
- Venue
- PLOS Pathogens
- Publisher
- Public Library of Science (PLoS)
- Published
- 2025-07-28
- Volume
- 21
- Issue
- 7
- Pages
- e1013363
- ISSN
- 1553-7366 (ISSN-L)
- 1553-7374
- PMC
- PMC12324677
- OpenAlex
- W4412727048
- Cited by
- 24
- References
- 47
- Citations by year
- 2026: 20 · 2025: 4
- FWCI
- 18.34
- Type
- journal article
- Language
- en
- Update notices
- new_version (2025-08-05)
- Open access
- gold
- doi.org
- Licence
- Locations
- PLoS Pathogens (publishedVersion, cc-by)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Research Foundation of Korea (RS-2021-NR058017, RS-2021-NR056582, RS-2025-00555365, RS-2025-02215093, RS-2022-NR072215, RS-2021-NF000550, RS-2024-00345184)
- Yonsei Signature Research Cluster Program (2025-22-0015)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Health Sciences › Medicine › Epidemiology › Fungal Infections and Studies
- Keywords
- Candida auris, calcineurin pathway, plasma membrane integrity, cell wall integrity, antifungal resistance, azole susceptibility, echinocandin resistance, virulence, fluconazole
- MeSH terms
- Thermotolerance, Candida auris, Animals, Antifungal Agents, Candidiasis, Cell Membrane, Cell Wall, Fungal Proteins, Virulence, Signal Transduction, Calcineurin, Drug Resistance, Fungal, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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