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Updated: Mar 12, 2026
CRISPR-mediated Genome Editing of the Human Fungal Pathogen Candida albicans
Published on: November 14, 2018
Mutational analysis of metacaspase CaMca1 and decapping activator Edc3 in the pathogenicity of Candida albicans
Jeong-Hoon Jeong1, Seok-Eui Lee1, Jinmi Kim1
1Department of Microbiology and Molecular Biology, College of Bioscience and Biotechnology, Chungnam National University, Daejeon 305-764, Republic of Korea.
Abstract:
Candida albicans, an opportunistic fungal pathogen, displays apoptotic cell death in response to various stresses and a wide range of antifungal treatments. CaMca1, which is the only metacaspase in C. albicans, has been described as a key player in apoptotic cell death. Edc3 is an mRNA decapping activator and a scaffold protein of processing bodies. Edc3 was previously shown to regulate CaMCA1 expression and oxidative stress-induced apoptosis. In this study, we analyzed the contribution of the catalytic residues of the CaMca1 to the oxidative stress-induced apoptosis and pathogenicity of C. albicans. The CaMCA1C292A mutation decreased caspase activity to a level similar to that observed in the Camca1/Camca1 deletion strain and over-expression of CaMCA1C292A failed to suppress the oxidative-stress phenotypes of the edc3/edc3 mutant strain. The edc3/edc3, Camca1/Camca1, and CaMCA1C292A mutant strains were not virulent in a murine candidiasis model. Filamentation defects were observed in the Camca1/Camca1 mutant cells, whereas this defect was only partial in CaMCA1C292A mutant cells. These results suggest that CaMca1 and Edc3 play essential roles in the oxidative stress-induced apoptosis and virulence of C. albicans, and also support the notion that Edc3 is a key regulator of CaMca1 expression.
Insights
Candida albicans metacaspase (CaMca1) and Edc3 are crucial for apoptosis and virulence. CaMca1
Area of Science:
- Mycology
- Molecular Biology
- Cell Biology
Background:
- Candida albicans, an opportunistic fungal pathogen, undergoes apoptosis.
- CaMca1 is the sole metacaspase in C. albicans and is implicated in apoptosis.
- Edc3 regulates CaMCA1 expression and oxidative stress-induced apoptosis.
Purpose of the Study:
- To investigate the role of CaMca1 catalytic residues in apoptosis and pathogenicity.
- To analyze the contribution of CaMca1 to oxidative stress-induced apoptosis and virulence.
- To elucidate the relationship between CaMca1 and Edc3 in C. albicans.
Main Methods:
- Site-directed mutagenesis of CaMCA1 (CaMCA1C292A).
- Assessment of caspase activity in mutant strains.
- Evaluation of virulence in a murine candidiasis model.
- Analysis of filamentation defects.
Main Results:
- The CaMCA1C292A mutation significantly reduced caspase activity.
- Over-expression of CaMCA1C292A did not rescue oxidative-stress phenotypes in edc3/edc3 mutants.
- Mutant strains (edc3/edc3, Camca1/Camca1, CaMCA1C292A) exhibited reduced or absent virulence.
- Camca1/Camca1 mutants showed filamentation defects, while CaMCA1C292A mutants had partial defects.
Conclusions:
- CaMca1 and Edc3 are essential for oxidative stress-induced apoptosis and virulence in C. albicans.
- Edc3 acts as a key regulator of CaMca1 expression.
- The catalytic activity of CaMca1 is critical for its role in apoptosis and pathogenicity.
