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首页> 美国卫生研究院文献>Infection and Immunity >Quorum-Sensing Escherichia coli Regulator A: a Regulator of the LysR Family Involved in the Regulation of the Locus of Enterocyte Effacement Pathogenicity Island in Enterohemorrhagic E. coli
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Quorum-Sensing Escherichia coli Regulator A: a Regulator of the LysR Family Involved in the Regulation of the Locus of Enterocyte Effacement Pathogenicity Island in Enterohemorrhagic E. coli

机译：法定人数的大肠杆菌调节剂A：LysR家族的调节剂参与调节大肠埃希氏菌中肠上皮细胞致病性岛的所在地

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The locus of enterocyte effacement (LEE) is a chromosomal pathogenicity island that encodes the proteins involved in the formation of the attaching and effacing lesions by enterohemorrhagic Escherichia coli (EHEC) and enteropathogenic E. coli (EPEC). The LEE comprises 41 open reading frames organized in five major operons, LEE1, LEE2, LEE3, tir (LEE5), and LEE4, which encode a type III secretion system, the intimin adhesin, the translocated intimin receptor (Tir), and other effector proteins. The first gene of LEE1 encodes the Ler regulator, which activates all the other genes within the LEE. We previously reported that the LEE genes were activated by quorum sensing through Ler (V. Sperandio, J. L. Mellies, W. Nguyen, S. Shin, and J. B. Kaper, Proc. Natl. Acad. Sci. USA 96:15196-15201, 1999). In this study we report that a putative regulator in the E. coli genome is itself activated by quorum sensing. This regulator is encoded by open reading frame b3243; belongs to the LysR family of regulators; is present in EHEC, EPEC, and E. coli K-12; and shares homology with the AphB and PtxR regulators of Vibrio cholerae and Pseudomonas aeruginosa, respectively. We confirmed the activation of b3243 by quorum sensing by using transcriptional fusions and renamed this regulator quorum-sensing E. coli regulator A (QseA). We observed that QseA activated transcription of ler and therefore of the other LEE genes. An EHEC qseA mutant had a striking reduction of type III secretion activity, which was complemented when qseA was provided in trans. Similar results were also observed with a qseA mutant of EPEC. The QseA regulator is part of the regulatory cascade that regulates EHEC and EPEC virulence genes by quorum sensing.
机译：肠上皮细胞外溢（LEE）的位点是一个染色体致病岛，编码与肠出血性大肠杆菌（EHEC）和肠致病性大肠杆菌（EPEC）形成附着和脱落的病变有关的蛋白质。 LEE包含41个开放阅读框，分为五个主要操纵子LEE1，LEE2，LEE3，tir（LEE5）和LEE4，它们编码III型分泌系统，内膜粘附素，易位的内膜受体（Tir）和其他效应子。蛋白质。 LEE1的第一个基因编码Ler调节剂，后者激活LEE内的所有其他基因。我们先前曾报道LE​​E基因是通过Ler（V. Sperandio，JL Mellies，W.Nguyen，S.Shin，and JB Kaper，Proc.Natl.Acad.Sci.USA 96：15196-15201，1999）通过群体感应激活的。 ）。在这项研究中，我们报告了大肠杆菌基因组中的推定调控因子本身是通过群体感应激活的。该调节器由开放阅读框b3243编码；属于LysR调节剂家族；存在于EHEC，EPEC和大肠杆菌K-12中；并分别与霍乱弧菌和铜绿假单胞菌的AphB和PtxR调节子同源。我们通过使用转录融合通过群体感应来确认b3243的激活，并重命名了该调控子群体感应大肠杆菌调控子A（QseA）。我们观察到QseA激活了ler的转录，因此也激活了其他LEE基因的转录。一个EHEC qseA突变体具有显着的III型分泌活性降低，而在 trans 中提供了 qseA 时，该突变体得到了补充。 EPEC的 qseA 突变体也观察到了相似的结果。 QseA调节剂是通过群体感应调节EHEC和EPEC毒力基因的调节级联的一部分。

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