Hierarchy in the expression of the locus of enterocyte effacement genes of enteropathogenic Escherichia coli

被引：135

作者：

Friedberg, D

Umanski, T

Fang, YA

Rosenshine, I

机构：

[1] Hebrew Univ Jerusalem, Fac Med, Dept Mol Genet, IL-91120 Jerusalem, Israel

[2] Hebrew Univ Jerusalem, Fac Med, Dept Biotechnol, IL-91120 Jerusalem, Israel

来源：

MOLECULAR MICROBIOLOGY | 1999年 / 34卷 / 05期

关键词：

D O I：

10.1046/j.1365-2958.1999.01655.x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Enteropathogenic Escherichia coli (EPEC) elicit changes in host cell morphology and cause actin rearrangement, a phenotype that has commonly been referred to as attaching/effacing (AE) lesions. The ability of EPEC to induce AE lesions is dependent upon a type III protein secretion/translocation system that is encoded by genes clustered in a 35.6 kb DNA segment, named the locus of enterocyte effacement (LEE). We used transcriptional fusions between the green fluorescent protein (gfp) reporter gene and LEE genes rorf2, orf3, orf5, escJ, escV and eae, together with immunoblot analysis with antibodies against Tir, intimin, EspB and EspF, to analyse the genetic regulation of the LEE. The expression of all these LEE genes was strictly dependent upon the presence of a functional integration host factor (IHF). IHF binds specifically upstream from the ler (orf1) promoter and appears to activate expression of ler, orf3, orf5 and rorf2 directly. The ler-encoded Ler protein was involved in activating the expression of escJ, escV, tir, eae, espB and espF. Expression of both IHF and Ler was needed to elicit actin rearrangement associated with AE lesions. In conclusion, IHF directly activates the expression of the ler and rorf2 transcriptional units, and Ler in turn mediates the expression of the other LEE genes.

引用

页码：941 / 952

页数：12

共 27 条

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