Sperandio Vanessa, Li Caiyi C, Kaper James B
Center for Vaccine Development and Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
Infect Immun. 2002 Jun;70(6):3085-93. doi: 10.1128/IAI.70.6.3085-3093.2002.
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.
肠上皮细胞脱落位点（LEE）是一个染色体致病岛，它编码由肠出血性大肠杆菌（EHEC）和肠致病性大肠杆菌（EPEC）形成紧密黏附损伤时所涉及的蛋白质。LEE由41个开放阅读框组成，这些开放阅读框被组织在五个主要操纵子中，即LEE1、LEE2、LEE3、tir（LEE5）和LEE4，它们编码一个III型分泌系统、紧密黏附素、易位紧密黏附素受体（Tir）以及其他效应蛋白。LEE1的第一个基因编码Ler调节因子，它激活LEE内的所有其他基因。我们之前报道过LEE基因通过群体感应经Ler激活（V. Sperandio、J. L. Mellies、W. Nguyen、S. Shin和J. B. Kaper，《美国国家科学院院刊》96:15196 - 15201，1999）。在本研究中，我们报道大肠杆菌基因组中的一个假定调节因子自身被群体感应激活。这个调节因子由开放阅读框b3243编码；属于LysR调节因子家族；存在于EHEC、EPEC和大肠杆菌K - 12中；并且分别与霍乱弧菌和铜绿假单胞菌的AphB和PtxR调节因子具有同源性。我们通过使用转录融合证实了群体感应对b3243的激活，并将这个调节因子重新命名为群体感应大肠杆菌调节因子A（QseA）。我们观察到QseA激活了ler的转录，进而激活了其他LEE基因的转录。一个EHEC qseA突变体的III型分泌活性显著降低，当反式提供qseA时这种降低得到了互补。在EPEC的qseA突变体中也观察到了类似结果。QseA调节因子是通过群体感应调节EHEC和EPEC毒力基因的调节级联反应的一部分。
