GSE133611
Deletion of the fungus specific protein phosphatase Z1 exaggerates the consequences of oxidative stress elicited by tert-butyl-hydroperoxide in Candida albicans (RNAseq data set)
Candida albicans is an opportunistic pathogen which is responsible for widespread nosocomial infections. It encompasses a fungus specific serine/threonine protein phosphatase gene CaPPZ1 that is involved in cation transport, cell wall integrity, oxidative stress response, morphological alterations, and virulence. We demonstrated that tert-butyl-hydoperoxide induced oxidative stress suppressed the growth rate and blocked the proliferation of the fungal cells without effecting their viability, both in the cappz1 KO mutant and in the genetically matching QMY23 control strains. To reveal the gene expression changes behind the above observation we carried out a global transcriptome analysis by DNA microarray hybridization as well as RNA sequencing, and confirmed our results by quantitative RT-PCR. The numbers of genes affected and the amplitudes of the transcript-level changes revealed that the deletion of CaPPZ1 enhances the effects of oxidative stress. Thus the roles of this fungus specific protein phosphatase in important physiological processes like membrane transport, cell surface interactions, oxidoreductase activity, cell signaling, translation, and RNA processing becomes more pronounced under oxidative conditions.  We conclude that in the wild type C. albicans CaPPZ1 has a protective role against oxidative damage, and suggest that the specific inhibition of this phosphatase combined with mild oxidative treatment could be a feasible approach of topical antifungal therapy. Overall design: Examination of untreated and 0.4 mM tBOOH-treated control and cappz1 mutant Candida albicans cultures in three- three replicates.