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Hydrogen peroxide-induced oxidative stress responses in Desulfovibrio vulgaris Hildenborough

机译:过氧化氢诱导的寻常脱硫弧菌希尔登伯勒的氧化应激反应

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To understand how sulphate-reducing bacteria respond to oxidative stresses, the responses of Desulfovibrio vulgaris Hildenborough to H_2O_2-induced stresses were investigated with transcriptomic, proteomic and genetic approaches. H_2O_2 and induced chemical species (e.g. polysulfide, ROS) and redox potential shift increased the expressions of the genes involved in detoxification, thioredoxin-dependent reduction system, protein and DNA repair, and decreased those involved in sulfate reduction, lactate oxidation and protein synthesis. A gene coexpression network analysis revealed complicated network interactions among differentially expressed genes, and suggested possible importance of several hypothetical genes in H_2O_2 stress. Also, most of the genes in PerR and Fur regulons were highly induced, and the abundance of a Fur regulon protein increased. Mutant analysis suggested that PerR and Fur are functionally overlapped in response to stresses induced by H_2O_2 and reaction products, and the upregulation of thioredoxin-dependent reduction genes was independent of PerR or Fur. It appears that induction of those stress response genes could contribute to the increased resistance of deletion mutants to H_2O_2-induced stresses. In addition, a conceptual cellular model of D. vulgaris responses to H_2O_2 stress was constructed to illustrate that this bacterium may employ a complicated molecular mechanism to defend against the H_2O_2-induced stresses.
机译:为了了解硫酸盐还原菌如何应对氧化应激,采用转录组学,蛋白质组学和遗传学方法研究了脱硫脱硫弧菌希尔登伯勒对H_2O_2诱导的胁迫的响应。 H_2O_2和诱导的化学物种(例如多硫化物,ROS)和氧化还原电位转移增加了与排毒,硫氧还蛋白依赖性还原系统,蛋白质和DNA修复有关的基因的表达,并减少了与硫酸盐还原,乳酸氧化和蛋白质合成有关的基因的表达。基因共表达网络分析揭示了差异表达基因之间复杂的网络相互作用,并暗示了几种假设基因在H_2O_2胁迫中的重要性。而且,PerR和Fur调节子中的大多数基因都被高度诱导,并且Fur调节子蛋白的丰度增加。突变分析表明,PerR和Fur在功能上重叠,以响应H_2O_2和反应产物诱导的应激,并且硫氧还蛋白依赖性还原基因的上调独立于PerR或Fur。似乎这些胁迫反应基因的诱导可能有助于删除突变体对H_2O_2诱导的胁迫的抗性增加。此外,构建了D. vulgaris对H_2O_2胁迫反应的概念性细胞模型,以说明该细菌可能利用复杂的分子机制来防御H_2O_2诱导的胁迫。

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