Vph2 is required for protection against a reductive stress in Candida albicans

Vph2 is a putative V-ATPase assembly factor. Our previous study has characterized its roles in localization of V-ATPase subunit, cell wall composition, hyphal development and virulence. In this study, our results further demonstrated that Vph2 was localized around the nucleus and in patches close to the periphery of the cell, indicating that Vph2 was located to the endoplasmic reticulum (ER), which was consistent with that in Saccharomyces cerevisiae. Disruption of VPH2 led to hypersensitivity to reducing stresses induced by dithiothreitol (DTT) and β-mercaptoethanol (β-ME), and displayed increased GSH content and up-regulation of unfolded protein response (UPR)-related genes, such as PRB1 and PMT4. However, the induced UPR and growth defect on β-ME plates of vph2Δ/Δ mutant could be partly alleviated by the GSH-specific scavenger 1-chloro-2, 4-dinitrobenzene (CDNB). These results indicated that loss of VPH2 led to an increase in GSH levels, which induced the UPR and caused the defective growth on reductive stress induced by β-ME. In summary, Vph2 is necessary to maintain resistance against reductive stresses. •Vph2 is located to the endoplasmic reticulum.•Disruption of VPH2 led to sensitivity to reducing stresses induced by DTT and β-ME.•The vph2Δ/Δ mutant displays increased GSH content.•Deletion of VPH2 causes up-regulation of UPR-related genes, such as PRB1 and PMT4.•The UPR and growth defect on β-ME plates can be partly alleviated by CDNB.