Copper (Cu) is a micronutrient necessary for proper growth and function of eukaryotic organisms. Although necessary, Cu can be toxic due to its ability to do Fenton-like chemistry and cause protein aggregation and as such is tightly regulated. Fungal organisms such as opportunistic pathogen Candida albicans (C. albicans) have developed efficient pathways to regulate Cu levels in response to changes in the host environment, including exposure to antifungal drugs. Using Size Exclusion Chromatography coupled with Inductively Coupled Plasma- Mass Spectrometry (SEC-ICP-MS), we have characterized changes in metalloprotein levels as a result of treating C. albicans cells in culture with an antifungal azole drug. We find significant changes in levels of copper-containing proteins, notably CuZn Superoxide dismutase1 (Sod1), the biggest client of Cu in the cytosol and important for handling reactive oxygen species, and the metallothionein Crd2. Here, we will discuss how these changes in metalloprotein status may impact susceptibility or tolerance of C. albicans antifungal drug stress.

Azole antifungal treatment leads to copper dyshomeostasis in opportunistic fungal pathogen Candida albicans

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