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.
复制标题
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
中科院分区:
文献类型:
--
作者:
Zhu,C;Agin,TS;Elliott,SJ;Johnson,LA;Thate,TE;Kaper,JB;Boedeker,EC
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.