• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >NikR Mediates Nickel-Responsive Transcriptional Repression of the Helicobacter pylori Outer Membrane Proteins FecA3 (HP1400) and FrpB4 (HP1512)
【24h】

NikR Mediates Nickel-Responsive Transcriptional Repression of the Helicobacter pylori Outer Membrane Proteins FecA3 (HP1400) and FrpB4 (HP1512)

机译：NikR介导幽门螺杆菌外膜蛋白FecA3（HP1400）和FrpB4（HP1512）的镍响应转录抑制。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The transition metal nickel plays an important role in gastric colonization and persistence of the important human pathogen Helicobacter pylori, as it is the cofactor of the abundantly produced acid resistance factor urease. Nickel uptake through the inner membrane is mediated by the NixA protein, and the expression of NixA is controlled by the NikR regulatory protein. Here we report that NikR also controls the nickel-responsive expression of the FecA3 (HP1400) and FrpB4 (HP1512) outer membrane proteins (OMPs), as well as the nickel-responsive expression of an ExbB-ExbD-TonB system, which may function in energization of outer membrane transport. Transcription and expression of the frpB4 and fecA3 genes were repressed by nickel in wild-type H. pylori 26695, but they were independent of nickel and derepressed in an isogenic nikR mutant. Both the frpB4 and fecA3 genes were transcribed from a promoter directly upstream of their start codon. Regulation by NikR was mediated via nickel-dependent binding to specific operators overlapping either the +1 or ?10 sequence in the frpB4 and fecA3 promoters, respectively, and these operators contained sequences resembling the proposed H. pylori NikR recognition sequence (TATWATT-N11-AATWATA). Transcription of the HP1339-1340-1341 operon encoding the ExbB2-ExbD2-TonB2 complex was also regulated by nickel and NikR, but not by Fur and iron. In conclusion, H. pylori NikR controls nickel-responsive expression of the HP1400 (FecA3) and HP1512 (FrpB4) OMPs. We hypothesize that these two NikR-regulated OMPs may participate in the uptake of complexed nickel ions and that this process is energized by the NikR-regulated ExbB2-ExbD2-TonB2 system, another example of the specific adaptation of H. pylori to the gastric lifestyle.
机译：过渡金属镍是重要人体病原体幽门螺杆菌在胃菌落和持久性中的重要作用，因为它是大量产生的抗酸因子脲酶的辅助因子。 NixA蛋白介导通过内膜吸收镍，NikR调节蛋白控制NixA的表达。在这里，我们报道NikR还控制FecA3（HP1400）和FrpB4（HP1512）外膜蛋白（OMP）的镍响应性表达，以及ExbB-ExbD-TonB系统的镍响应性表达，该功能可能起作用激励外膜运输。镍在野生型 H中抑制了 frpB4 和 fecA3 基因的转录和表达。 pylori 26695，但它们独立于镍，并在同基因的 nikR 突变体中被抑制。 frpB4 和 fecA3 基因均从其起始密码子上游的启动子转录而来。 NikR的调控是通过镍依赖性结合特定的操纵子来实现的，这些操纵子分别与 frpB4 和 fecA3 启动子中的+1或？10序列重叠，并且这些操纵子包含序列类似于建议的 H。幽门螺杆菌NikR识别序列（TATWATT-N 11 -AATWATA）。编码ExbB2-ExbD2-TonB2复合物的HP1339-1340-1341操纵子的转录也受镍和NikR的调节，但不受Fur和铁的调节。总之， H。幽门螺杆菌NikR控制着HP1400（FecA3）和HP1512（FrpB4）OMP的镍响应性表达。我们假设这两个NikR调节的OMP可能参与络合镍离子的吸收，并且该过程由NikR调节的ExbB2-ExbD2-TonB2系统激发，这是 H的特殊适应性的另一个例子。幽门螺杆菌

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号