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Organic Hydroperoxide Induces Prodigiosin Biosynthesis in Serratia sp. ATCC 39006 in an OhrR-Dependent Manner

机译:有机氢过氧化物以 OhrR 依赖性方式诱导沙雷氏菌 ATCC 39006 的原粘菌素生物合成

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摘要

The biosynthesis of prodigiosin in the model prodigiosin-producing strain, Serratia sp. ATCC 39006, is significantly influenced by environmental and cellular signals. However, a comprehensive regulatory mechanism for this process has not been well established. In the present study, we demonstrate that organic hydroperoxide activates prodigiosin biosynthesis in an OhrR-dependent manner. Specifically, the MarR-family transcriptional repressor OhrR (Ser39006_RS05455) binds to its operator located far upstream of the promoter region of the prodigiosin biosynthesis operon (319 to 286 nucleotides (ntj upstream of the transcription start site) and negatively regulates the expression of prodigiosin biosynthesis genes. Organic hydroperoxide disassociates the binding between OhrR and its operator, thereby promoting the prodigiosin production. Moreover, OhrR modulates the resistance of Serratia sp. ATCC 39006 to organic hydroperoxide by regulating the transcription of its own gene and the downstream cotranscribed ohr gene. These results demonstrate that OhrR is a pleiotropic repressor that modulates the prodigiosin production and the resistance of Serratia sp. ATCC 39006 to organic hydroperoxide stress. IMPORTANCE Bacteria naturally encounter various environmental and cellular stresses. Organic hydroperoxides generated from the oxidation of polyunsaturated fatty acids are widely distributed and usually cause lethal oxidative stress by damaging cellular components. OhrR is known as a regulator that modulates the resistance of bacteria to organic hydroperoxide stress. In the current study, organic hydroperoxide disassociates OhrR from the promoter of prodigiosin biosynthesis gene cluster, thus promoting transcription of pigA to -0 genes. In this model, organic hydroperoxide acts as an inducer of prodigiosin synthesis in Serratia sp. ATCC 39006. These results improve our understanding of the regulatory network of prodigiosin synthesis and serve as an example for identifying the cross talk between the stress responses and the regulation of secondary metabolism.
机译:产原菌素模型菌株沙雷氏菌属 ATCC 39006 中原体苷的生物合成受环境和细胞信号的显着影响。然而,这一过程的综合监管机制尚未建立。在本研究中,我们证明了有机氢过氧化物以 OhrR 依赖性方式激活 prodigiosin 生物合成。具体而言,MarR 家族转录阻遏蛋白 OhrR (Ser39006_RS05455) 与其位于原菌素生物合成操纵子启动子区域(319 至 286 个核苷酸(转录起始位点上游的 ntj))上游的载体结合,并负向调节原菌素生物合成基因的表达。有机氢过氧化物使 OhrR 与其操作子之间的结合解离,从而促进原菌素的产生。此外,OhrR 通过调节其自身基因和下游共转录的 OHR 基因的转录来调节沙雷氏菌 ATCC 39006 对有机过氧化氢的抗性。这些结果表明,OhrR 是一种多效性阻遏因子,可调节沙雷氏菌 ATCC 39006 对有机氢过氧化物胁迫的原菌素产生和抗性。重要性:细菌自然会遇到各种环境和细胞压力。多不饱和脂肪酸氧化产生的有机氢过氧化物分布广泛,通常通过破坏细胞成分引起致命的氧化应激。OhrR 被称为调节细菌对有机过氧化氢胁迫的抵抗力的调节剂。在目前的研究中,有机氢过氧化物将OhrR与prodigiosin生物合成基因簇的启动子分离,从而促进pigA转录为-0基因。在该模型中,有机氢过氧化氢作为沙雷氏菌 ATCC 39006 中原菌素合成的诱导剂。这些结果提高了我们对原菌素合成调控网络的理解,并为识别应激反应与次生代谢调控之间的串扰提供了参考。

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