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The cloned locus of enterocyte effacement from enterohemorrhagic Escherichia coli O157:H7 is unable to confer the attaching and effacing phenotype upon E. coli K-12.从肠出血性大肠杆菌O157:H7克隆出的肠细胞脱落位点无法使大肠杆菌K-12产生紧密黏附与脱落表型。
Infect Immun. 1999 Aug;67(8):4260-3. doi: 10.1128/IAI.67.8.4260-4263.1999.
2
Complete nucleotide sequence and analysis of the locus of enterocyte Effacement from rabbit diarrheagenic Escherichia coli RDEC-1.兔致腹泻性大肠杆菌RDEC-1肠细胞脱落位点的全核苷酸序列及分析
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3
The Per regulon of enteropathogenic Escherichia coli : identification of a regulatory cascade and a novel transcriptional activator, the locus of enterocyte effacement (LEE)-encoded regulator (Ler).肠致病性大肠杆菌的Per调控子：调控级联和新型转录激活因子——肠细胞脱落位点（LEE）编码调控因子（Ler）的鉴定
Mol Microbiol. 1999 Jul;33(2):296-306. doi: 10.1046/j.1365-2958.1999.01473.x.
4
Characterization of the eaeA gene from rabbit enteropathogenic Escherichia coli strain RDEC-1 and comparison to other eaeA genes from bacteria that cause attaching-effacing lesions.兔肠道致病性大肠杆菌RDEC-1 eaeA基因的特性分析及其与其他导致紧密黏附损伤的细菌的eaeA基因的比较。
FEMS Microbiol Lett. 1996 Nov 1;144(2-3):249-58. doi: 10.1111/j.1574-6968.1996.tb08538.x.
5
A mosaic pathogenicity island made up of the locus of enterocyte effacement and a pathogenicity island of Escherichia coli O157:H7 is frequently present in attaching and effacing E. coli.由肠细胞脱落位点和大肠杆菌O157:H7的一个致病岛组成的嵌合致病岛经常存在于黏附性和脱落性大肠杆菌中。
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Positive effects of multiple pch genes on expression of the locus of enterocyte effacement genes and adherence of enterohaemorrhagic Escherichia coli O157 : H7 to HEp-2 cells.多个pch基因对肠上皮细胞脱落基因表达以及肠出血性大肠杆菌O157∶H7黏附HEp-2细胞的积极作用。
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Mutation of toxB and a truncated version of the efa-1 gene in Escherichia coli O157:H7 influences the expression and secretion of locus of enterocyte effacement-encoded proteins but not intestinal colonization in calves or sheep.大肠杆菌O157:H7中toxB基因的突变以及efa-1基因的截短版本会影响肠细胞脱落位点编码蛋白的表达和分泌，但不影响在犊牛或绵羊中的肠道定植。
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本文引用的文献

1
The Per regulon of enteropathogenic Escherichia coli : identification of a regulatory cascade and a novel transcriptional activator, the locus of enterocyte effacement (LEE)-encoded regulator (Ler).肠致病性大肠杆菌的Per调控子：调控级联和新型转录激活因子——肠细胞脱落位点（LEE）编码调控因子（Ler）的鉴定
Mol Microbiol. 1999 Jul;33(2):296-306. doi: 10.1046/j.1365-2958.1999.01473.x.
2
Enteropathogenic and enterohaemorrhagic Escherichia coli: more subversive elements.肠致病性大肠杆菌和肠出血性大肠杆菌：更多的破坏因素。
Mol Microbiol. 1998 Dec;30(5):911-21. doi: 10.1046/j.1365-2958.1998.01144.x.
3
Molecular evolution of a pathogenicity island from enterohemorrhagic Escherichia coli O157:H7.肠出血性大肠杆菌O157:H7致病岛的分子进化
Infect Immun. 1998 Aug;66(8):3810-7. doi: 10.1128/IAI.66.8.3810-3817.1998.
4
EPEC delivers the goods.
Trends Microbiol. 1998 May;6(5):169-72; discussion 172-3. doi: 10.1016/s0966-842x(98)01266-9.
5
The complete sequence of the locus of enterocyte effacement (LEE) from enteropathogenic Escherichia coli E2348/69.肠致病性大肠杆菌E2348/69的肠细胞脱落位点（LEE）的完整序列。
Mol Microbiol. 1998 Apr;28(1):1-4. doi: 10.1046/j.1365-2958.1998.00783.x.
6
A novel EspA-associated surface organelle of enteropathogenic Escherichia coli involved in protein translocation into epithelial cells.一种与肠致病性大肠杆菌 EspA 相关的新型表面细胞器，参与蛋白质转运至上皮细胞。
EMBO J. 1998 Apr 15;17(8):2166-76. doi: 10.1093/emboj/17.8.2166.
7
Diarrheagenic Escherichia coli.致泻性大肠杆菌
Clin Microbiol Rev. 1998 Jan;11(1):142-201. doi: 10.1128/CMR.11.1.142.
8
Enteropathogenic E. coli (EPEC) transfers its receptor for intimate adherence into mammalian cells.肠道致病性大肠杆菌（EPEC）将其紧密黏附受体转移至哺乳动物细胞中。
Cell. 1997 Nov 14;91(4):511-20. doi: 10.1016/s0092-8674(00)80437-7.
9
Versatile insertion plasmids for targeted genome manipulations in bacteria: isolation, deletion, and rescue of the pathogenicity island LEE of the Escherichia coli O157:H7 genome.用于细菌靶向基因组操作的多功能插入质粒：大肠杆菌O157:H7基因组致病岛LEE的分离、缺失及拯救
J Bacteriol. 1997 Jul;179(13):4426-8. doi: 10.1128/jb.179.13.4426-4428.1997.
10
A cloned pathogenicity island from enteropathogenic Escherichia coli confers the attaching and effacing phenotype on E. coli K-12.从肠致病性大肠杆菌克隆出的一个致病岛赋予了大肠杆菌K-12紧密黏附与抹平样病变表型。
Mol Microbiol. 1997 Jan;23(2):399-407. doi: 10.1046/j.1365-2958.1997.2311591.x.

从肠出血性大肠杆菌O157:H7克隆出的肠细胞脱落位点无法使大肠杆菌K-12产生紧密黏附与脱落表型。

The cloned locus of enterocyte effacement from enterohemorrhagic Escherichia coli O157:H7 is unable to confer the attaching and effacing phenotype upon E. coli K-12.

作者信息

Elliott S J, Yu J, Kaper J B

机构信息

Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.

出版信息

Infect Immun. 1999 Aug;67(8):4260-3. doi: 10.1128/IAI.67.8.4260-4263.1999.

DOI:10.1128/IAI.67.8.4260-4263.1999
PMID:10417201
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC96734/
Abstract

The locus of enterocyte effacement (LEE) pathogenicity island of enterohemorrhagic Escherichia coli (EHEC) O157:H7 possesses the same genes in identical order and orientation as the LEE of enteropathogenic E. coli (EPEC) O127:H6 but is unable to form attaching and effacing (A/E) lesions or to secrete Esp proteins when it is cloned in an E. coli K-12 background. The A/E phenotype could not be restored by trans complementation with a variety of cloned EPEC LEE fragments, suggesting functional and/or regulatory differences between the LEE pathogenicity islands of EPEC O127:H6 and EHEC O157:H7.

摘要

肠出血性大肠杆菌（EHEC）O157:H7的肠细胞损伤位点（LEE）致病岛与肠致病性大肠杆菌（EPEC）O127:H6的LEE具有相同顺序和方向的相同基因，但当它克隆于大肠杆菌K-12背景中时，无法形成紧密黏附与抹平（A/E）损伤或分泌Esp蛋白。用多种克隆的EPEC LEE片段进行反式互补无法恢复A/E表型，这表明EPEC O127:H6和EHEC O157:H7的LEE致病岛之间存在功能和/或调控差异。