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Acid-Induced Activation of the Urease Promoters Is Mediated Directly by the ArsRS Two-Component System of Helicobacter pylori

机译:幽门螺杆菌的ArsRS两组分系统直接介导尿素酶启动子的酸诱导激活。

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The nickel-containing enzyme urease is an essential colonization factor of the human gastric pathogen Helicobacter pylori which enables the bacteria to survive the low-pH conditions of the stomach. Transcription of the urease genes is positively controlled in response to increasing concentrations of nickel ions and acidic pH. Here we demonstrate that acid-induced transcription of the urease genes is mediated directly by the ArsRS two-component system. Footprint analyses identify binding sites of the phosphorylated ArsR response regulator within the ureA and ureI promoters. Furthermore, deletion of a distal upstream ArsR binding site of the ureA promoter demonstrates its role in acid-dependent activation of the promoter. In addition, acid-induced transcription of the ureA gene is unaltered in a nikR mutant, providing evidence that pH-responsive regulation and nickel-responsive regulation of the ureA promoter are mediated by independent mechanisms involving the ArsR response regulator and the NikR protein.
机译:含镍酶脲酶是人胃病原体幽门螺杆菌的必不可少的定居因子,可使细菌在胃的低pH条件下存活。响应于镍离子浓度的增加和酸性pH的增加,尿素酶基因的转录受到了积极的控制。在这里,我们证明了酸诱导的脲酶基因转录是直接由ArsRS两组分系统介导的。足迹分析确定了 ureA ureI 启动子中磷酸化ArsR反应调节剂的结合位点。此外,删除 ureA 启动子的远端上游ArsR结合位点表明了其在启动子的酸依赖性激活中的作用。此外,在 nikR 突变体中,酸诱导的 ureA 基因的转录没有改变,这提供了 ureA的pH响应调节和镍响应调节的证据。 启动子由涉及ArsR反应调节剂和NikR蛋白的独立机制介导。

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