Molecular evolution of a pathogenicity island from enterohemorrhagic Escherichia coli O157:H7
Molecular evolution of a pathogenicity island from enterohemorrhagic Escherichia coli O157:H7
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DOI：
10.1128/iai.66.8.3810-3817.1998
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发表时间：
1998-08-01
影响因子：
3.1
通讯作者：
Blattner, FR
中科院分区：
文献类型：
--
作者：
Perna, NT;Mayhew, GF;Blattner, FR
我们报告的完整的43,359 bp的基因座的肠上皮细胞消失（LEE）从EDL 933，肠出血性大肠杆菌O 157：H7血清型最初从受污染的汉堡包中分离的出血性结肠炎的爆发牵连。用同源重组驱动的靶向载体从EDL 933染色体分离该基因座。最近完成的LEE序列从肠致病性E。coli（EPEC）E2348/69为比较分析整个毒力岛提供了机会。我们在EDL 933 LEE中共识别出54个开放阅读帧。其中，13属于一个假定的P4家族原噬菌体命名为933 L，原噬菌体是不存在于E2348/69，但发现在密切相关的EPEC O 55：H7血清型和其他O 157：H7分离株，其余41个基因是由两个完整的LEE共享，我们描述的性质和程度的变化，两个菌株之间的每个基因。发散率沿轨迹沿着是不均匀的。大多数基因在两种菌株之间显示出大于95%的同一性，但其他基因的变化超过了大肠杆菌菌株之间克隆分歧的预期。这些高度分歧的基因中的几个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加上自然选择，并为我们理解的相互作用的病原体与其主机，为O 157：H7的出现，并为病原体的进化史一般的影响。
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.