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.
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。
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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
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