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.
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