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首页> 外文期刊>Infection and immunity >The Nickel-Responsive Regulator NikR Controls Activation and Repression of Gene Transcription in Helicobacter pylori
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The Nickel-Responsive Regulator NikR Controls Activation and Repression of Gene Transcription in Helicobacter pylori

机译：镍响应性调节器NIKR控制幽门螺杆菌基因转录的激活和抑制

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The NikR protein is a nickel-dependent regulatory protein which is a member of the ribbon-helix-helix family of transcriptional regulators. The gastric pathogen Helicobacter pylori expresses a NikR ortholog, which was previously shown to mediate regulation of metal metabolism and urease expression, but the mechanism governing the diverse regulatory effects had not been described until now. In this study it is demonstrated that NikR can regulate H. pylori nickel metabolism by directly controlling transcriptional repression of NixA-mediated nickel uptake and transcriptional induction of urease expression. Mutation of the nickel uptake gene nixA in an H. pylori 26695 nikR mutant restored the ability to grow in Brucella media supplemented with 200 μM NiCl2 but did not restore nickel-dependent induction of urease expression. Nickel-dependent binding of NikR to the promoter of the nixA gene resulted in nickel-repressed transcription, whereas nickel-dependent binding of NikR to the promoter of the ureA gene resulted in nickel-induced transcription. Subsequent analysis of NikR binding to the nixA and ureA promoters showed that the regulatory effect was dependent on the location of the NikR-recognized binding sequence. NikR recognized the region from ?13 to +21 of the nixA promoter, encompassing the +1 and ?10 region, and this binding resulted in repression of nixA transcription. In contrast, NikR bound to the region from ?56 to ?91 upstream of the ureA promoter, resulting in induction of urease transcription. In conclusion, the NikR protein is able to function both as a repressor and as an activator of gene transcription, depending on the position of the binding site.
机译：Nikr蛋白是依赖于镍依赖性调节蛋白，其是带状螺旋 - 螺旋系列转录调节剂的成员。胃病原体幽门螺杆菌幽门螺杆菌表达尼克尔垂直表道，前面显示出介导金属代谢和脲酶表达的调节，但目前尚未描述控制各种调节效应的机制。在这项研究中，证明尼克尔可以调节 H.幽门螺杆菌镍代谢通过直接控制尼西介导的镍介导的镍吸收和尿素表达转录诱导的转录抑制。镍吸收基因 Nixa 在 H中的突变。 Pylori 26695 Nikr 突变体恢复了在补充有200μmnICl 2 的Brucella培养基中生长的能力，但未恢复依赖于尿素表达的依赖性诱导。尼克尔依赖于尼克尔依赖于 nixa 基因的启动子，导致镍抑制转录，而Nikr的镍依赖性结合到尿素的启动子，导致了镍诱导的转录。随后分析尼克尔与 NIXA 和尿素启动子的分析表明，调节效果取决于尼克尔公认的结合序列的位置。尼克尔认识到 nixa 启动子的13至+21的区域，包括+1和10区，并且这种结合导致抑制 nixa 转录。相比之下，尼克尔与α56到α91的区域绑定到尿素启动子上游，导致释放脲酶转录。总之，尼克尔蛋白能够作为阻遏物和基因转录的活化剂，这取决于结合位点的位置。

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