Deciphering the regulatory mechanisms of the cAMP/protein kinase A pathway and their roles in the pathogenicity of Candida auris
Open accessAbstract
The emergence of multidrug-resistant fungal pathogens is a significant concern for global public health. Candida auris poses a considerable threat as a multidrug-resistant fungal pathogen. Our recent study revealed that the adenylyl cyclase Cyr1 and protein kinase A (PKA) pathways play distinct and redundant roles in drug resistance and pathogenicity of C. auris . However, the upstream and negative feedback regulatory mechanisms of C. auris are not yet fully understood. In this study, we discovered that the small GTPase Ras1, along with its nucleotide exchange factor Cdc25 and GTPase-activating protein Ira2, plays a major role in regulating cAMP/PKA-dependent traits, while G-protein-coupled receptor Gpr1 and heterotrimeric G-protein α subunit Gpa2 play a minor role. Pde2 plays a major role in negative feedback regulation of the cAMP/PKA pathway, while Pde1 plays a minor role. Hyperactivation of the Ras/cAMP/PKA pathway by deleting PDE2 or BCY1 renders C. auris cells thermosensitive and susceptible to nutrient deficiency, which leads to attenuated virulence. Our study demonstrates the distinct contributions of hyperactivation of the Ras/cAMP/PKA signaling pathway to C. auris pathogenesis and suggests potential therapeutic targets for C. auris- mediated candidiasis. IMPORTANCE: Candida auris is a major concern as a multidrug-resistant fungal pathogen. While our previous studies highlighted the crucial roles of the cAMP/protein kinase A (PKA) pathway in regulating drug resistance, stress responses, morphogenesis, ploidy change, biofilm formation, and pathogenicity in this pathogen, their regulatory mechanism remains unclear. In our study, we provided evidence that the cAMP/PKA signaling pathway in C. auris is primarily governed by the small GTPase RAS rather than a G-protein-coupled receptor. Additionally, we discovered that the negative feedback regulation of cAMP, controlled by phosphodiesterases, is vital for C. auris virulence by promoting resistance to high temperatures and nutrient deficiencies. These findings underscore the diverse pathobiological significance of the Ras/cAMP/PKA signaling pathway in C. auris , shedding light on potential therapeutic targets and strategies for combating this multidrug-resistant fungal pathogen.
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In other fungal species, bicarbonate plays critical roles in energy metabolism and morphogenesis through the cAMP/PKA signaling pathway that converges at the regulator Efg1.
“In other fungal species, bicarbonate plays critical roles in energy metabolism and morphogenesis, as it is acting through the cyclic adenosine monophosphate–dependent protein kinase A (cAMP/PKA) signaling pathway that converges at the regulator Efg1 (refs. 23–25).”
From Candida auris skin tropism and antifungal resistance are mediated by carbonic anhydrase Nce103 (2025) · cites this paper as [25]
The Introduction (page unavailable) links cAMP/PKA signaling to pseudohyphae formation, and the Results (page unavailable) link it to glycogen accumulation, an aspect of energy storage. The paper does not establish that bicarbonate acts through this pathway or that the pathway converges at Efg1 (searched: bicarbonate, Efg1, energy metabolism, and morphogenesis). (LLM, conf=0.79)
Experimental — accuracy not yet measuredDeletion of CYR1, RAS1 and CDC25 in strain AR387 increases AMB tolerance.
“Deletion of CYR1, RAS1 and CDC25 in strain AR387 increases AMB tolerance23,25 (Extended Data Fig. 3h)”
From Candida auris skin tropism and antifungal resistance are mediated by carbonic anhydrase Nce103 (2025) · cites this paper as [25]
The Results (Ras1 is the primary upstream regulator; page unavailable) report increased AMB tolerance after CYR1 or RAS1 deletion. Another Results section says the CDC25 deletion mutant had a stress-response pattern similar to the RAS1 mutant, but does not explicitly identify increased AMB tolerance. The reported mutants were constructed in strain B8441, not AR387. (LLM, conf=0.89)
Experimental — accuracy not yet measuredHyperactivation of the Ras/cAMP/PKA pathway by BCY1 or PDE2 deletion attenuated the virulence during murine systemic infection by reducing the ability to thrive in nutrient-deficient conditions.
“Furthermore, hyperactivation of the Ras/cAMP/PKA pathway by BCY1 or PDE2 deletion attenuated the virulence during murine systemic infection by reducing the ability to thrive in nutrient-deficient conditions [79,80].”
From Host–Candida auris interactions in the skin (2026) · cites this paper as [79]
The Results sections report reduced virulence in mice after PDE2 deletion and reduced survival under nutrient-starved conditions after BCY1 or PDE2 deletion; the paper also reports attenuated virulence after BCY1 deletion. But the Discussion says impaired survival under nutrient starvation *may* reduce virulence and identifies other potentially relevant effects. It does not establish nutrient-starvation sensitivity as the cause of the reduced virulence. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe C. auris cAMP/PKA signaling pathway is important for biofilm formation.
“The C. auris cAMP/PKA signaling pathway has been shown to be important for biofilm formation (59, 60).”
From The <i>Candida auris</i> Hog1 MAP kinase is essential for the colonization of murine skin and intradermal persistence (2024) · cites this paper as [60]
C. 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 [79]
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- Authors
- Kim, J.-S., Lee, K.-T., & Bahn, Y.-S.
- Affiliations
- Yonsei University (KR)
- Korea Zoonosis Research Institute, Jeonbuk National University
- Corresponding author
- Bahn, Yong-Sun
- Venue
- Microbiology Spectrum
- Publisher
- American Society for Microbiology
- Published
- 2023-10-17
- Volume
- 11
- Issue
- 5
- Pages
- e0215223-e0215223
- ISSN
- 2165-0497 (ISSN-L)
- PMC
- PMC10581177
- OpenAlex
- W4386467338
- Cited by
- 24
- References
- 44
- Citations by year
- 2026: 9 · 2025: 6 · 2024: 7 · 2023: 2
- FWCI
- 2.13
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Microbiology Spectrum (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Research Foundation of Korea (2021R1A2B5B03086596, 2022R1A4A3022401, 2022R1C1C2003274)
- Korea Health Industry Development Institute (HI22C1987, HI20C0326)
- 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 auris, cAMP/PKA signaling, Ras1, negative feedback regulation, PDE1, Gpa2, Cdc25, IRA2, virulence, thermosensitivity, nutritional deficiency, multidrug resistance, candidiasis, therapeutic target
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