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Comparative analyses of how diverse pathogenic bacteria combat the potential for secretion-associated stress.

机译:比较分析各种致病细菌如何抵抗与分泌有关的压力的潜力。

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摘要

Secretins are a family of outer membrane pore-forming proteins that are critical for virulence-related Type 2 and Type 3 secretion systems, as well as Type 4 pili biogenesis and filamentous phage export in Gram-negative bacteria. Although secretins normally localize in the outer membrane they can sometimes mislocalize and cause bacterial cell stress. This stress is specifically alleviated by the widely conserved phage-shock-protein (Psp) system. The Psp system is present in numerous bacterial species. However, some bacteria use secretins but do not have the Psp system. In order to provide a global understanding of how two different organisms Yersinia enterocolitica (Psp +) and Pseudomonas aeruginosa (Psp-) might deal with the potential for secretin-induced stress, random transposon mutagenesis and microarray studies were undertaken. This revealed that in the model Psp+ species Y. enterocolitica the Psp proteins were necessary and sufficient for tolerating secretin-induced stress. However, in the model Psp- species P. aeruginosa there was no transcriptional response to secretin-induced stress. Nevertheless, transposon insertion in four different loci rendered P. aeruginosa hypersensitive to secretin production. One of these loci (PA0943) encoded a protein that was shown to be important for localization of the XcpQ secretin, a component of a Type 2 secretion system, to the outer membrane. Therefore, deletion of PA0943 led to a defect in the export of several important Type 2 secretion substrates. Taken together, all of these data suggest that P. aeruginosa lacks an equivalent of the Psp stress-response system. Instead, P. aeruginosa may prevent secretin mislocalization stress from occurring. Mutations, such as a PA0943 disruption, may cause elevated secretin stress to which P. aeruginosa cannot respond. Consistent with this, providing the P. aeruginosa mutant with critical Psp components alleviated the secretin-sensitivity. In summary, with regard to secretin-induced stress, Y. enterocolitica employs a response strategy whereas P. aeruginosa may rely on prevention.
机译:促胰液素是外膜成孔蛋白家族,对于与毒力相关的2型和3型分泌系统,以及4型菌毛生物发生和革兰氏阴性细菌中的丝状噬菌体输出至关重要。尽管促胰液素通常位于外膜中,但它们有时可能会错位并引起细菌细胞应激。广泛保存的噬菌体休克蛋白(Psp)系统可特别缓解这种压力。 Psp系统存在于多种细菌中。但是,某些细菌使用促胰液素,但没有Psp系统。为了提供对两种不同生物体小肠结肠炎耶尔森氏菌(Psp +)和铜绿假单胞菌(Psp-)可能如何处理促胰液素诱导的应激的潜力的全球理解,进行了随机转座子诱变和微阵列研究。这表明在模型Psp +种小肠结肠炎耶尔森氏菌中,Psp蛋白对于耐受促胰液素诱导的应激是必要的和充分的。然而,在模型Psp-种铜绿假单胞菌中,没有针对促胰液素诱导的应激的转录反应。然而,在四个不同基因座中的转座子插入使铜绿假单胞菌对促胰液素的产生高度敏感。这些基因座之一(PA0943)编码一种蛋白质,该蛋白质对于XcpQ分泌蛋白(一种2型分泌系统的成分)对外膜的定位非常重要。因此,PA0943的缺失导致几种重要的2型分泌底物的出口出现缺陷。综上所述,所有这些数据表明铜绿假单胞菌缺乏与Psp应激反应系统相当的系统。相反,铜绿假单胞菌可防止促胰液素错误定位的压力发生。突变(例如PA0943破坏)可能会导致促分泌素升高,而铜绿假单胞菌无法应对。与此相一致,为铜绿假单胞菌突变体提供关键的Psp成分可减轻促胰液素的敏感性。总之,关于促胰液素诱导的应激,小肠结肠炎耶尔森氏菌采用一种应对策略,而铜绿假单胞菌可能依赖于预防。

著录项

  • 作者

    Seo, Jin.;

  • 作者单位

    New York University.;

  • 授予单位 New York University.;
  • 学科 Biology Microbiology.
  • 学位 Ph.D.
  • 年度 2009
  • 页码 191 p.
  • 总页数 191
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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