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Updated: Aug 1, 2026
Bio-energetics Investigation of Candida albicans Using Real-time Extracellular Flux Analysis
Published on: March 19, 2019
Pathogenicity of 5-fluorocytosine resistant strains of Candida albicans
M O Fasoli1, D Kerridge, J F Ryley
1Department of Biochemistry, Cambridge, UK.
Abstract:
Mutants of Candida albicans blocked in pyrimidine transport and salvage metabolism were produced by a two step mutagenic procedure and selected by their resistance to 5-fluorocytosine (flucytosine). The growth rates and growth yields of these mutants did not differ significantly from the parental strain of C. albicans. Examination of their pathogenicity to mice demonstrated that a defect in the uridine transport function decreased the pathogenicity of C. albicans.
Insights
Researchers created Candida albicans mutants defective in pyrimidine metabolism. A defect in uridine transport significantly reduced the fungus
Area of Science:
- Mycology
- Molecular Biology
- Biochemistry
Background:
- Candida albicans is an opportunistic fungal pathogen.
- Pyrimidine metabolism is crucial for fungal growth and survival.
- 5-fluorocytosine (flucytosine) is an antifungal drug targeting pyrimidine synthesis.
Purpose of the Study:
- To generate and characterize Candida albicans mutants with defects in pyrimidine transport and salvage pathways.
- To investigate the role of pyrimidine metabolism in C. albicans pathogenicity.
Main Methods:
- A two-step mutagenic procedure was employed to generate mutants.
- Mutants were selected based on resistance to 5-fluorocytosine.
- Pathogenicity was assessed in a mouse model.
Main Results:
- Mutants with blocked pyrimidine transport and salvage pathways were successfully generated.
- These mutants exhibited growth rates and yields comparable to the parental strain.
- A defect in uridine transport specifically decreased the pathogenicity of C. albicans in mice.
Conclusions:
- Pyrimidine transport, particularly uridine uptake, is essential for the full virulence of Candida albicans.
- Targeting pyrimidine salvage pathways could be a potential strategy for antifungal therapy.
