Institute for Microbiology, Ernst-Moritz-Arndt-University of Greifswald, D-17487 Greifswald, Germany.
Mol Cell Proteomics. 2011 Nov;10(11):M111.009506. doi: 10.1074/mcp.M111.009506. Epub 2011 Jul 11.
Protein S-thiolation is a post-translational thiol-modification that controls redox-sensing transcription factors and protects active site cysteine residues against irreversible oxidation. In Bacillus subtilis the MarR-type repressor OhrR was shown to sense organic hydroperoxides via formation of mixed disulfides with the redox buffer bacillithiol (Cys-GlcN-Malate, BSH), termed as S-bacillithiolation. Here we have studied changes in the transcriptome and redox proteome caused by the strong oxidant hypochloric acid in B. subtilis. The expression profile of NaOCl stress is indicative of disulfide stress as shown by the induction of the thiol- and oxidative stress-specific Spx, CtsR, and PerR regulons. Thiol redox proteomics identified only few cytoplasmic proteins with reversible thiol-oxidations in response to NaOCl stress that include GapA and MetE. Shotgun-liquid chromatography-tandem MS analyses revealed that GapA, Spx, and PerR are oxidized to intramolecular disulfides by NaOCl stress. Furthermore, we identified six S-bacillithiolated proteins in NaOCl-treated cells, including the OhrR repressor, two methionine synthases MetE and YxjG, the inorganic pyrophosphatase PpaC, the 3-D-phosphoglycerate dehydrogenase SerA, and the putative bacilliredoxin YphP. S-bacillithiolation of the OhrR repressor leads to up-regulation of the OhrA peroxiredoxin that confers together with BSH specific protection against NaOCl. S-bacillithiolation of MetE, YxjG, PpaC and SerA causes hypochlorite-induced methionine starvation as supported by the induction of the S-box regulon. The mechanism of S-glutathionylation of MetE has been described in Escherichia coli also leading to enzyme inactivation and methionine auxotrophy. In summary, our studies discover an important role of the bacillithiol redox buffer in protection against hypochloric acid by S-bacillithiolation of the redox-sensing regulator OhrR and of four enzymes of the methionine biosynthesis pathway.
蛋白质 S-巯基化是一种翻译后巯基修饰,可控制氧化还原感应转录因子,并防止活性位点半胱氨酸残基发生不可逆氧化。在枯草芽孢杆菌中,MarR 型阻遏物 OhrR 被证明可以通过与氧化还原缓冲剂 bacillithiol(Cys-GlcN-Malate,BSH)形成混合二硫键来感知有机氢过氧化物,这种修饰被称为 S-bacillithiolation。在这里,我们研究了强氧化剂次氯酸在枯草芽孢杆菌中引起的转录组和氧化还原蛋白质组的变化。次氯酸钠应激的表达谱表明存在二硫键应激,因为硫和氧化应激特异性 Spx、CtsR 和 PerR 调控子被诱导。硫醇氧化还原蛋白质组学仅鉴定了少数细胞质蛋白,这些蛋白在应对次氯酸钠应激时发生可逆的硫醇氧化,其中包括 GapA 和 MetE。Shotgun 液相色谱-串联 MS 分析表明,GapA、Spx 和 PerR 被次氯酸钠应激氧化为分子内二硫键。此外,我们在经次氯酸钠处理的细胞中鉴定了六个 S-bacillithiolated 蛋白,包括 OhrR 阻遏物、两个甲硫氨酸合酶 MetE 和 YxjG、无机焦磷酸酶 PpaC、3-D-磷酸甘油酸脱氢酶 SerA 和假定的芽孢杆菌还原酶 YphP。OhrR 阻遏物的 S-bacillithiolation 导致 OhrA 过氧化物酶的上调,与 BSH 一起赋予枯草芽孢杆菌对次氯酸钠的特异性保护。MetE、YxjG、PpaC 和 SerA 的 S-bacillithiolation 导致次氯酸盐诱导的蛋氨酸饥饿,这得到 S-box 调控子的诱导支持。大肠杆菌中 MetE 的 S-谷胱甘肽化机制也已被描述,导致酶失活和蛋氨酸营养缺陷。总之,我们的研究发现了 bacillithiol 氧化还原缓冲液在通过 OhrR 氧化还原感应调节剂的 S-bacillithiolation 以及甲硫氨酸生物合成途径的四个酶的 S-bacillithiolation 来保护枯草芽孢杆菌免受次氯酸中的重要作用。