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调控因子协同开启肠出血性大肠杆菌O157:H7中LEE基因的表达:Ler、GrlA、HNS和RpoS之间的相互作用

Concert of regulators to switch on LEE expression in enterohemorrhagic Escherichia coli O157:H7: interplay between Ler, GrlA, HNS and RpoS.

作者信息

Laaberki Maria-Halima, Janabi Nazila, Oswald Eric, Repoila Francis

机构信息

UMR1225 IHAP-INRA/ENVT, 23 Chemin des Capelles, F-31070 Toulouse, France.

出版信息

Int J Med Microbiol. 2006 Aug;296(4-5):197-210. doi: 10.1016/j.ijmm.2006.02.017. Epub 2006 Apr 17.

DOI:10.1016/j.ijmm.2006.02.017
PMID:16618552
Abstract

Enterohemorrhagic (EHEC) and enteropathogenic (EPEC) Escherichia coli strains carry a pathogenicity island termed locus of enterocyte effacement (LEE) responsible for attaching and effacing lesions on epithelial cells. The expression of LEE varies among isolates and is dependent on environmental cues. In the EHEC O157:H7 Sakaï isolate (RIMD-0509952 strain), we found that the non-coding RNA, DsrA, activates the expression of the LEE. This activation requires RpoS, the stress sigma factor. The DsrA/RpoS regulatory pathway mediates its positive effect by stimulating the transcription of ler, a positive regulatory gene encoded by the LEE. A second regulatory pathway, repressed by HNS, is also able to activate the transcription of ler and requires GrlA, another LEE-encoded regulator. Both regulatory pathways, DsrA/RpoS and HNS/GrlA, affect the activity of the ler distal promoter and require the Ler protein to be functional. Our data demonstrate that the LEE expression can be turned on by at least two separate pathways acting on the transcription of ler.

摘要

肠出血性大肠杆菌(EHEC)和肠致病性大肠杆菌(EPEC)菌株携带一个称为肠细胞脱落位点(LEE)的致病岛,该致病岛负责在上皮细胞上形成黏附和脱落性病变。LEE的表达在不同分离株中有所不同,并取决于环境信号。在EHEC O157:H7阪崎分离株(RIMD-0509952菌株)中,我们发现非编码RNA DsrA可激活LEE的表达。这种激活需要应激σ因子RpoS。DsrA/RpoS调控途径通过刺激ler(LEE编码的一个正向调控基因)的转录来介导其正向作用。另一条受HNS抑制的调控途径也能够激活ler的转录,并且需要另一个LEE编码的调控因子GrlA。DsrA/RpoS和HNS/GrlA这两条调控途径均影响ler远端启动子的活性,并且需要Ler蛋白发挥功能。我们的数据表明,LEE的表达可通过至少两条作用于ler转录的独立途径开启。

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