Abstract

Our letter reports a hitherto unrecognized role of Pdr16 in modulating the antifungal susceptibility of Candida auris to different drugs, especially azoles. Deletion of PDR16 resulted in a 4-fold decrease in the MIC for azoles, while ectopic overexpression of this protein reduced susceptibility to different classes of antifungal drugs, including azoles, amphotericin B, and 5-fluorocytosine (5FC). The data suggest that PDR16 expression levels in clinical isolates could serve as a surrogate marker to predict antifungal resistance traits.