Tir tyrosine phosphorylation and pedestal formation are delayed in enteropathogenic Escherichia coli sepZ::TnphoA mutant 30-5-1(3)

被引：12

作者：

DeVinney, R

Nisan, I

Ruschkowski, S

Rosenshine, I

Finlay, BB ^{[1
]}

机构：

[1] Univ British Columbia, Biotechnol Lab, Vancouver, BC V6T 1Z3, Canada

[2] Hebrew Univ Jerusalem, Dept Mol Genet, IL-91120 Jerusalem, Israel

[3] Hebrew Univ Jerusalem, Dept Biotechnol, IL-91120 Jerusalem, Israel

[4] Hebrew Univ Jerusalem, Dept Clin Microbiol, IL-91120 Jerusalem, Israel

来源：

INFECTION AND IMMUNITY | 2001年 / 69卷 / 01期

关键词：

D O I：

10.1128/IAI.69.1.559-563.2001

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Enteropathogenic Escherichia call (EPEC) strain 30-5-1(3) has been reported to form attaching and effacing (A/E) lesions without Tir tyrosine phosphorylation. In this study, we show that 30-5-1(3), which has a transposon insertion within the sepZ gene, forms wild-type A/E lesions including Tir tyrosine phosphorylation, but at a slower rate. A/E lesion formation by 30-5-1(3) occurs without detectable secretion of Tir or other EPEC Esp secreted proteins.

引用

页码：559 / 563

页数：5

共 24 条

[21] A pathogenic bacterium triggers epithelial signals to form a functional bacterial receptor that mediates actin pseudopod formation [J].