Deng W, Li Y, Vallance B A, Finlay B B
Biotechnology Laboratory, University of British Columbia, Vancouver, British Columbia, V6T 1Z3, Canada.
Infect Immun. 2001 Oct;69(10):6323-35. doi: 10.1128/IAI.69.10.6323-6335.2001.
The family of attaching and effacing (A/E) bacterial pathogens, which includes diarrheagenic enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC), remains a significant threat to human and animal health. These bacteria intimately attach to host intestinal cells, causing the effacement of brush border microvilli. The genes responsible for this phenotype are encoded in a pathogenicity island called the locus of enterocyte effacement (LEE). Citrobacter rodentium is the only known murine A/E pathogen and serves as a small animal model for EPEC and EHEC infections. Here we report the full DNA sequence of C. rodentium LEE and provide a comparative analysis with the published LEEs from EPEC, EHEC, and the rabbit diarrheagenic E. coli strain RDEC-1. Although C. rodentium LEE shows high similarities throughout the entire sequence and shares all 41 open reading frames with the LEE from EPEC, EHEC, and RDEC-1, it is unique in its location of the rorf1 and rorf2/espG genes and the presence of several insertion sequences (IS) and IS remnants. The LEE of EPEC and EHEC is inserted into the selC tRNA gene. In contrast, the Citrobacter LEE is flanked on one side by an operon encoding an ABC transport system, and an IS element and sequences homologous to Shigella plasmid R100 and EHEC pO157 flank the other. The presence of plasmid sequences next to C. rodentium LEE suggests that the prototype LEE resided on a horizontally transferable plasmid. Additional sequence analysis reveals that the 3-kb plasmid in C. rodentium is nearly identical to p9705 in EHEC O157:H7, suggesting that horizontal plasmid transfer among A/E pathogens has occurred. Our results indicate that the LEE has been acquired by C. rodentium and A/E E. coli strains independently during evolution.
紧密黏附和消除性（A/E）细菌病原体家族，包括致腹泻性肠致病性大肠杆菌（EPEC）和肠出血性大肠杆菌（EHEC），仍然对人类和动物健康构成重大威胁。这些细菌紧密附着于宿主肠道细胞，导致刷状缘微绒毛消失。负责这种表型的基因编码在一个称为肠细胞消除位点（LEE）的致病岛中。鼠柠檬酸杆菌是唯一已知的鼠类A/E病原体，是EPEC和EHEC感染的小动物模型。在此，我们报告了鼠柠檬酸杆菌LEE的完整DNA序列，并与已发表的来自EPEC、EHEC和兔致腹泻性大肠杆菌菌株RDEC-1的LEE进行了比较分析。尽管鼠柠檬酸杆菌LEE在整个序列中显示出高度相似性，并且与来自EPEC、EHEC和RDEC-1的LEE共享所有41个开放阅读框，但它在rorf1和rorf2/espG基因的位置以及几个插入序列（IS）和IS残余物的存在方面是独特的。EPEC和EHEC的LEE插入到selC tRNA基因中。相比之下，柠檬酸杆菌的LEE一侧由编码ABC转运系统的操纵子侧翼，另一侧由与志贺氏菌质粒R100和EHEC pO157同源的IS元件和序列侧翼。鼠柠檬酸杆菌LEE旁边存在质粒序列表明原型LEE存在于水平可转移的质粒上。进一步的序列分析表明，鼠柠檬酸杆菌中的3 kb质粒与EHEC O157:H7中的p9705几乎相同，这表明A/E病原体之间发生了水平质粒转移。我们的结果表明，LEE在进化过程中已被鼠柠檬酸杆菌和A/E大肠杆菌菌株独立获得。
