Complete nucleotide sequence and analysis of the locus of enterocyte Effacement from rabbit diarrheagenic Escherichia coli RDEC-1.

Complete nucleotide sequence and analysis of the locus of enterocyte Effacement from rabbit diarrheagenic Escherichia coli RDEC-1.
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兔致泻性大肠杆菌 RDEC-1 肠上皮细胞消失的完整核苷酸序列和位点分析。

DOI:
10.1128/iai.69.4.2107-2115.2001
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发表时间:
2001
影响因子:
3.1
通讯作者:
Boedeker,EC
Boedeker,EC
中科院分区:
医学2区
文献类型:
--
作者:
Zhu,C;Agin,TS;Elliott,SJ;Johnson,LA;Thate,TE;Kaper,JB;Boedeker,EC

文献摘要

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致病性岛被称为肠细胞湮没位点(LEE),存在于与人类和其他动物腹泻相关的多种附着和湮没病原体中。为了探讨LEE序列变异与宿主特异性和遗传谱系的关系,我们测定了家兔腹泻致病菌大肠杆菌RDEC-1 (O15:H−)LEE区域的核苷酸序列,并与人致病菌LEE区域的核苷酸序列进行了比较。大肠杆菌(EPEC, O127:H6)和肠出血。大肠杆菌(EHEC, O157:H7)菌株。与EPEC和EHEC LEE不同,RDEC-1 LEE不选择性插入,两侧有一个IS2元件和lifatoxin基因。RDEC-1 LEE包含一个40个开放阅读帧的核心区域,所有这些区域都与EPEC和EHEC的LEE共享。在EHEC和EPEC的LEEs中存在的orf3和ERIC(肠重复基因间一致)序列在RDEC-1的LEEs中不存在。lee1、LEE2、LEE3、tir和lee4操作子的预测启动子在LEEs中是高度保守的,尽管上游区域对于cruciallee1启动子有很大的差异,表明在调控上存在差异。在共享基因中,在预测的氨基酸水平上,rdec1与EPEC和EHEC LEEs的III型分泌器、Ces伴侣和Ler调节因子的成分具有高度的同源性(>95%的同源性)。相比之下,在编码参与宿主相互作用的蛋白质(如内膜素(Eae)和分泌蛋白(Tir和Esps))的基因中观察到更多的差异(66%至88%的一致性)。比较了来自RDEC-1的高度可变基因与来自感染不同物种和不同进化谱系的附着和清除病原体的基因。尽管RDEC-1与一些人类感染的EPEC和EHEC不同,但观察到的大多数变异似乎是由于进化谱系而不是宿主特异性。因此,许多观察到的与发病机制有关的基因的高变异性可能并不代表对不同宿主物种的特异性适应。
The pathogenicity island termed the locus of enterocyte effacement (LEE) is found in diverse attaching and effacing pathogens associated with diarrhea in humans and other animal species. To explore the relation of variation in LEE sequences to host specificity and genetic lineage, we determined the nucleotide sequence of the LEE region from a rabbit diarrheagenicEscherichia colistrain RDEC-1 (O15:H−) and compared it with those from human enteropathogenicE. coli(EPEC, O127:H6) and enterohemorrhagicE. coli(EHEC, O157:H7) strains. Differing from EPEC and EHEC LEEs, the RDEC-1 LEE is not inserted atselCand is flanked by an IS2 element and thelifAtoxin gene. The RDEC-1 LEE contains a core region of 40 open reading frames, all of which are shared with the LEE of EPEC and EHEC.orf3and the ERIC (enteric repetitive intergenic consensus) sequence present in the LEEs of EHEC and EPEC are absent from the RDEC-1 LEE. The predicted promoters ofLEE1, LEE2, LEE3, tir, andLEE4operons are highly conserved among the LEEs, although the upstream regions varied considerably fortirand the crucialLEE1promoter, suggesting differences in regulation. Among the shared genes, high homology (>95% identity) between the RDEC-1 and the EPEC and EHEC LEEs at the predicted amino acid level was observed for the components of the type III secretion apparatus, the Ces chaperones, and the Ler regulator. In contrast, more divergence (66 to 88% identity) was observed in genes encoding proteins involved in host interaction, such as intimin (Eae) and the secreted proteins (Tir and Esps). A comparison of the highly variable genes from RDEC-1 with those from a number of attaching and effacing pathogens infecting different species and of different evolutionary lineages was performed. Although RDEC-1 diverges from some human-infecting EPEC and EHEC, most of the variation observed appeared to be due to evolutionary lineage rather than host specificity. Therefore, much of the observed hypervariability in genes involved in pathogenesis may not represent specific adaptation to different host species.