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Iron-Responsive Repression of Urease Expression in Helicobacter hepaticus Is Mediated by the Transcriptional Regulator Fur

机译:转录调节因子介导的铁反应性抑制肝组织中的尿素酶表达。

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Persistent colonization of mucosal surfaces by bacteria in the mammalian host requires concerted expression of colonization factors, depending on the environmental conditions. Helicobacter hepaticus is a urease-positive pathogen that colonizes the intestinal and hepatobiliary tracts of rodents. Here it is reported that urease expression of H. hepaticus is iron repressed by the transcriptional regulator Fur. Iron restriction of growth medium resulted in a doubling of urease activity in wild-type H. hepaticus strain ATCC 51449 and was accompanied by increased levels of urease subunit proteins and ureA mRNA. Insertional inactivation of the fur gene abolished iron-responsive repression of urease activity, whereas inactivation of the perR gene did not affect iron-responsive regulation of urease activity. The iron-responsive promoter element was identified directly upstream of the H. hepaticus ureA gene. Recombinant H. hepaticus Fur protein bound to this ureA promoter region in a metal-dependent matter, and binding resulted in the protection of a 41-bp, Fur box-containing operator sequence located at positions ?35 to ?75 upstream of the transcription start site. In conclusion, H. hepaticus Fur controls urease expression at the transcriptional level in response to iron availability. This represents a novel type of urease regulation in ureolytic bacteria and extends the already diverse regulatory repertoire of the Fur protein.
机译:哺乳动物宿主中细菌在粘膜表面的持久定殖需要定殖因子的一致表达,具体取决于环境条件。 Helicobacter hepaticus 是一种脲酶阳性的病原体,可定居在啮齿动物的肠和肝胆道中。此处报道了 H的脲酶表达。转录调控因子Fur抑制肝中的铁。铁对生长培养基的限制导致野生型 H中脲酶活性加倍。肝细胞株ATCC 51449,并伴有尿素酶亚基蛋白和 ureA mRNA水平的升高。 fur 基因的插入失活消除了铁酶对尿素酶活性的抑制,而 perR 基因的失活不影响铁响应的尿素酶活性的调节。在 H的上游直接鉴定出铁反应性启动子元件。肝ureA 基因。重组 H。肝 Fur蛋白以金属依赖性物质与该 ureA 启动子区域结合,结合后可保护位于第35位的含有Fur盒的41 bp操纵基因序列。在转录起始位点上游〜75。总之, H。肝 Fur响应铁的有效性而在转录水平上控制脲酶的表达。这代表了尿素分解细菌中新型的脲酶调节,并扩展了Fur蛋白已经多样化的调节范围。

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