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首页> 外文期刊>Infection and immunity >The Locus of Enterocyte Effacement (LEE)-Encoded Regulator Controls Expression of Both LEE- and Non-LEE-Encoded Virulence Factors in Enteropathogenic and EnterohemorrhagicEscherichia coli
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The Locus of Enterocyte Effacement (LEE)-Encoded Regulator Controls Expression of Both LEE- and Non-LEE-Encoded Virulence Factors in Enteropathogenic and EnterohemorrhagicEscherichia coli

机译：肠上皮细胞浸润（LEE）编码调节剂的位点控制肠道致病性和肠出血性大肠杆菌中LEE和非LEE编码毒力因子的表达

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Regulation of virulence gene expression in enteropathogenicEscherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) is incompletely understood. In EPEC, the plasmid-encoded regulator Per is required for maximal expression of proteins encoded on the locus of enterocyte effacement (LEE), and a LEE-encoded regulator (Ler) is part of the Per-mediated regulatory cascade upregulating the LEE2, LEE3, andLEE4 promoters. We now report that Ler is essential for the expression of multiple LEE-located genes in both EPEC and EHEC, including those encoding the type III secretion pathway, the secreted Esp proteins, Tir, and intimin. Ler is therefore central to the process of attaching and effacing (AE) lesion formation. Ler also regulates the expression of LEE-located genes not required for AE-lesion formation, including rorf2, orf10,rorf10, orf19, and espF, indicating that Ler regulates additional virulence properties. In addition, Ler regulates the expression of proteins encoded outside the LEE that are not essential for AE lesion formation, including TagA in EHEC and EspC in EPEC. Δler mutants of both EPEC and EHEC show altered adherence to epithelial cells and express novel fimbriae. Ler is therefore a global regulator of virulence gene expression in EPEC and EHEC.
机译：肠致病性大肠埃希氏菌和肠出血性大肠杆菌中毒力基因表达的调控。大肠杆菌（EHEC）尚未完全了解。在EPEC中，质粒编码的调节剂Per是最大程度表达在肠上皮细胞消失（LEE）部位编码的蛋白质的必要条件，而LEE编码的调节剂（Ler）是Per介导的调节级联反应的一部分，可上调 LEE2 ， LEE3 和 LEE4 启动子。现在，我们报道Ler对于在EPEC和EHEC中表达多个LEE定位的基因至关重要，包括那些编码III型分泌途径，分泌的Esp蛋白，Tir和intimin的基因。因此，Ler对于附着和消失（AE）病变形成过程至关重要。 Ler还调节AE病变形成不需要的LEE定位基因的表达，包括 rorf2 ， orf10 ， rorf10 ， orf19 和 espF ，表明Ler调节其他毒力特性。此外，Ler调节在LEE外部编码的蛋白质的表达，这些蛋白质对于AE病变形成不是必需的，包括EHEC中的TagA和EPEC中的EspC。 EPEC和EHEC的Δ ler 突变体均表现出对上皮细胞的粘附性改变，并表达新的菌毛。因此，Ler是EPEC和EHEC中毒力基因表达的全球调节者。

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