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肠出血性大肠杆菌O157:H7致病岛的分子进化

Molecular evolution of a pathogenicity island from enterohemorrhagic Escherichia coli O157:H7.

作者信息

Perna N T, Mayhew G F, Pósfai G, Elliott S, Donnenberg M S, Kaper J B, Blattner F R

机构信息

Laboratory of Genetics, University of Wisconsin-Madison, Madison Wisconsin 53706, USA.

出版信息

Infect Immun. 1998 Aug;66(8):3810-7. doi: 10.1128/IAI.66.8.3810-3817.1998.

DOI:10.1128/IAI.66.8.3810-3817.1998
PMID:9673266
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC108423/
Abstract

We report the complete 43,359-bp sequence of the locus of enterocyte effacement (LEE) from EDL933, an enterohemorrhagic Escherichia coli O157:H7 serovar originally isolated from contaminated hamburger implicated in an outbreak of hemorrhagic colitis. The locus was isolated from the EDL933 chromosome with a homologous-recombination-driven targeting vector. Recent completion of the LEE sequence from enteropathogenic E. coli (EPEC) E2348/69 afforded the opportunity for a comparative analysis of the entire pathogenicity island. We have identified a total of 54 open reading frames in the EDL933 LEE. Of these, 13 fall within a putative P4 family prophage designated 933L. The prophage is not present in E2348/69 but is found in a closely related EPEC O55:H7 serovar and other O157:H7 isolates. The remaining 41 genes are shared by the two complete LEEs, and we describe the nature and extent of variation among the two strains for each gene. The rate of divergence is heterogeneous along the locus. Most genes show greater than 95% identity between the two strains, but other genes vary more than expected for clonal divergence among E. coli strains. Several of these highly divergent genes encode proteins that are known to be involved in interactions with the host cell. This pattern suggests recombinational divergence coupled with natural selection and has implications for our understanding of the interaction of both pathogens with their host, for the emergence of O157:H7, and for the evolutionary history of pathogens in general.

摘要

我们报道了来自肠出血性大肠杆菌O157:H7血清型EDL933的肠细胞脱落位点(LEE)的完整43359碱基对序列,该菌株最初从一起出血性结肠炎暴发中受污染的汉堡中分离得到。通过同源重组驱动的靶向载体从EDL933染色体中分离出该位点。近期完成的肠致病性大肠杆菌(EPEC)E2348/69的LEE序列为对整个致病岛进行比较分析提供了机会。我们在EDL933的LEE中总共鉴定出54个开放阅读框。其中,13个位于一个推定的P4家族原噬菌体中,命名为933L。该原噬菌体在E2348/69中不存在,但在密切相关的EPEC O55:H7血清型和其他O157:H7分离株中存在。其余41个基因由两个完整的LEE共享,我们描述了每个基因在两个菌株之间的变异性质和程度。沿该位点的分歧率是异质的。大多数基因在两个菌株之间显示出大于95%的同一性,但其他基因的变异比大肠杆菌菌株间克隆分歧预期的要大。其中几个高度分歧的基因编码已知参与与宿主细胞相互作用的蛋白质。这种模式表明重组分歧与自然选择相结合,对我们理解这两种病原体与宿主的相互作用、O157:H7的出现以及病原体的一般进化史具有启示意义。

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A third secreted protein that is encoded by the enteropathogenic Escherichia coli pathogenicity island is required for transduction of signals and for attaching and effacing activities in host cells.肠道致病性大肠杆菌致病岛编码的第三种分泌蛋白是宿主细胞信号转导以及紧密黏附与抹平活性所必需的。
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