Essential Role of Erg6p in Maintaining Oxidative Stress Tolerance and Iron Homeostasis in .

The human pathogenic fungus is the second leading cause of candidemia, a life-threatening invasive mycosis. Clinical outcomes are complicated by reduced susceptibility of to azoles together with its ability to evolve stable resistance to both azoles and echinocandins following drug exposure. Compared to other spp., displays robust oxidative stress resistance. In this study, we investigated the impact of gene deletion on the oxidative stress response in gene encodes sterol-24-C-methyltransferase, which is involved in the final steps of ergosterol biosynthesis. Our previous results showed that the mutant has a lower ergosterol content in its membranes. Here, we show that the mutant displays increased susceptibility to oxidative stress inducing agents, such as menadione, hydrogen peroxide and diamide, accompanied with increased intracellular ROS production. The mutant is not able to tolerate higher concentrations of iron in the growth media. We observed increased expression of transcription factors, Yap1p, Msn4p and Yap5p, together with increased expression of catalase encoding the gene and vacuolar iron transporter in the mutant cells. However, it seems that the gene deletion does not influence the function of mitochondria.