Molecular Biology Division, Bhabha Atomic Research Centre, Mumbai 400 085, India.
J Biosci. 2021;46.
The highly radiation-resistant bacterium responds to gamma radiation or desiccation through the coordinated expression of genes belonging to Radiation and Desiccation Resistance/Response (RDR) regulon. RDR regulon is operated through -acting sequence RDRM (Radiation Desiccation Response Motif), -acting repressor DdrO and protease IrrE (also called PprI). The present study evaluated whether RDR regulon controls the response of to various other DNA damaging stressors, to which it is resistant, such as UV rays, mitomycin C (MMC), methyl methanesulfonate (MMS), ethidium bromide (EtBr), etc. Activation of 3 RDR regulon genes (B, B and DR1143) was studied by tagging their promoter sequences with a highly sensitive GFP reporter. Here we demonstrated that all the DNA damaging stressors elicited activation of RDR regulon of in a dose-dependent and RDRM-/IrrE-dependent manner. However, ROS-mediated indirect effects [induced by hydrogen peroxide (HO), methyl viologen (MV), heavy metal/metalloid (zinc or tellurite), etc.] did not activate RDR regulon. We also showed that level of activation was inversely proportional to cellular abundance of repressor DdrO. Our data strongly suggests that direct DNA damage activates RDR regulon in .
高度耐辐射细菌通过协调表达属于辐射和干燥抗性/响应(RDR)调控子的基因对γ辐射或干燥作出反应。RDR 调控子通过作用序列 RDRM(辐射干燥响应基序)、作用抑制剂 DdrO 和蛋白酶 IrrE(也称为 PprI)来运作。本研究评估了 RDR 调控子是否控制了该细菌对其他各种抵抗的 DNA 损伤应激源的反应,这些应激源包括紫外线、丝裂霉素 C(MMC)、甲基甲烷磺酸酯(MMS)、溴化乙锭(EtBr)等。通过用高度敏感的 GFP 报告基因标记其启动子序列来研究 3 个 RDR 调控子基因(B、B 和 DR1143)的激活。在这里,我们证明了所有的 DNA 损伤应激源都以剂量依赖和 RDRM-/IrrE 依赖的方式引发了 的 RDR 调控子的激活。然而,ROS 介导的间接效应(由过氧化氢(HO)、甲紫精(MV)、重金属/类金属(锌或碲酸盐)等引起)并没有激活 RDR 调控子。我们还表明,激活水平与抑制剂 DdrO 的细胞丰度成反比。我们的数据强烈表明,直接的 DNA 损伤激活了 中的 RDR 调控子。