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Updated: Jun 4, 2026

CRISPR-mediated Genome Editing of the Human Fungal Pathogen Candida albicans
Published on: November 14, 2018
Rad52 function prevents chromosome loss and truncation in Candida albicans
E Andaluz1, A Bellido, J Gómez-Raja
1Departamento de Ciencias Biomédicas, Area Microbiología, Facultad de Ciencias, Universidad de Extremadura, 06071 Badajoz, Spain.
Rad52 protein is crucial for maintaining genomic stability in Candida albicans. Deleting RAD52 significantly increases loss of heterozygosity and chromosomal instability, similar to cancer cells.
Area of Science:
- Microbiology
- Genetics
- Molecular Biology
Background:
- RAD52 plays a key role in recombination in Saccharomyces cerevisiae.
- Candida albicans is an important fungal pathogen with heterozygous loci.
- Genomic stability is critical for pathogenic microorganisms.
Purpose of the Study:
- To investigate the role of Rad52 in maintaining genomic stability in Candida albicans.
- To assess the impact of RAD52 deletion on loss of heterozygosity (LOH) and chromosomal instability (CIN).
Main Methods:
- Utilizing the HIS4 heterozygosity in Candida albicans SC5314.
- Generating and analyzing rad52-deletion (rad52-ΔΔ) strains.
- Quantifying LOH rates and assessing genomic alterations including chromosome loss and breakage.
Main Results:
- rad52-ΔΔ strains showed a >100-fold increase in LOH rate at HIS4 compared to Rad52+ strains.
- All analyzed rad52-ΔΔ auxotrophs exhibited LOH, including whole chromosome loss or truncation with telomere addition.
- rad52-ΔΔ strains displayed significant chromosomal instability (CIN), which was reversible upon RAD52 reintroduction.
Conclusions:
- RAD52 is essential for suppressing LOH and maintaining genomic stability in Candida albicans.
- The observed CIN in rad52-ΔΔ strains resembles genomic instability found in human cancers.
- These findings support the mutator hypothesis, suggesting CIN facilitates further mutations and aneuploidies.
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