Mistranslation accelerates the evolution of antifungal drug resistance in Candida albicans [CGH]

The fungal pathogen Candida albicans and other pathogens of the CTG clade reassigned the leucine CUG codon to serine and tolerate highly variable levels of both serine and leucine at CUG positions in response to environmental cues. Previous studies found that increased leucine misincorporation levels enhance resistance to drugs but the underlying mechanisms are not known. To clarify the biological role of this tuneable codon ambiguity, we evolved C. albicans strains engineered to mistranslate CUG at elevated levels, in the presence and absence of the antifungal drug fluconazole CGH analysis was performed on evolved C.albicans strains grown in presence of fluconazole and the parental strain not subjected to fluconazole.