Effect of deletion or overexpression of SisPerR on gene expression of Saccharolobus islandicus REY15A in the presence of H2O2

Sensing of ROS is essential for cellular response to oxidative stress. While oxidative stress response in bacteria and eukaryotes has been extensively studied, less is known about the mechanism in archaea. In this study, we demonstrate that deletion of sisperR, a gene encoding the PerR of the model hyperthermophilic archaeon Saccharolobus islandicus abolishes the oxidative stress-induced expression of a large number of genes. ΔsisperR exhibits enhanced tolerance to H2O2 treatment. Consistently, SisPerR overexpression leads to hypersensitivity to of the cells to the H2O2 treatment. We show that the expression of Dps and MntH which are involved in the regulation of cellular metal ion homeostasis, but not that of ROS scavenging enzymes, is significantly up-regulated with H2O2 treatment and repressed by SisPerR. In summary, this study has established that SisPerR is a repressive redox-sensing transcription factor regulating the intracellular metal ion homeostasis in Saccharolobus islandicus for the oxidative stress defense. To investigate the function of the FurR family protein SisPerR in the regulation of gene transcription in response to H2O2, we constructed Sisfha deletion and expression of S. islandicus and treated with H2O2. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells, the wild type strain E233S and Δsisfha, treated or mock-treated with NQO for 6 h.