Putting E-coli on a pedestal:: a unique system to study signal transduction and the actin cytoskeleton

被引：46

作者：

Goosney, DL ^{[1
]}

de Grado, M

Finlay, BB

机构：

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

[2] Univ British Columbia, Dept Biochem & Mol Biol, Vancouver, BC V6T 1Z3, Canada

[3] Univ British Columbia, Dept Microbiol & Immunol, Vancouver, BC V6T 1Z3, Canada

来源：

TRENDS IN CELL BIOLOGY | 1999年 / 9卷 / 01期

基金：

加拿大自然科学与工程研究理事会; 英国医学研究理事会;

关键词：

D O I：

10.1016/S0962-8924(98)01418-4

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Enteropathogenic Escherichia coli (EPEC) subverts host signalling pathways and the cytoskeleton during infection, resulting in disease characterized by diarrhoea. Recent studies have revolutionized our understanding of the infection process by showing that this bacterium inserts its own receptor into the plasma membrane overlying the host actin cytoskeleton. The reorganized actin forms a pedestal-like structure with the bacterium at the tip. This review discusses the mechanism of infection and pedestal formation and how this system might be a powerful tool for studying actin dynamics at the plasma membrane.

引用

页码：11 / 14

页数：4

共 36 条

[1] Increased levels of intracellular calcium are not required for the formation of attaching and effacing lesions by enteropathogenic and enterohemorrhagic Escherichia coli [J].

Bain, C ;

Keller, R ;

Collington, GK ;

Trabulsi, LR ;

Knutton, S .

INFECTION AND IMMUNITY, 1998, 66 (08) :3900-3908

[2] PROTEIN-PHOSPHORYLATION BY PROTEIN KINASE-C IN HEP-2 CELLS INFECTED WITH ENTEROPATHOGENIC ESCHERICHIA-COLI [J].

BALDWIN, TJ ;

BROOKS, SF ;

KNUTTON, S ;

HERNANDEZ, HAM ;

AITKEN, A ;

WILLIAMS, PH .

INFECTION AND IMMUNITY, 1990, 58 (03) :761-765

[3] CALCIUM-CALMODULIN DEPENDENCE OF ACTIN ACCRETION AND LETHALITY IN CULTURED HEP-2 CELLS INFECTED WITH ENTEROPATHOGENIC ESCHERICHIA-COLI [J].

BALDWIN, TJ ;

LEEDELAUNAY, MB ;

KNUTTON, S ;

WILLIAMS, PH .

INFECTION AND IMMUNITY, 1993, 61 (02) :760-763

[4] ELEVATION OF INTRACELLULAR FREE CALCIUM LEVELS IN HEP-2 CELLS INFECTED WITH ENTEROPATHOGENIC ESCHERICHIA-COLI [J].

BALDWIN, TJ ;

WARD, W ;

AITKEN, A ;

KNUTTON, S ;

WILLIAMS, PH .

INFECTION AND IMMUNITY, 1991, 59 (05) :1599-1604

[5] Agents that inhibit Rho, Rac, and Cdc42 do not block formation of actin pedestals in HeLa cells infected with enteropathogenic Escherichia coli [J].

Ben-Ami, G ;

Ozeri, V ;

Hanski, E ;

Hofmann, F ;

Aktories, K ;

Hahn, KM ;

Bokoch, GM ;

Rosenshine, I .

INFECTION AND IMMUNITY, 1998, 66 (04) :1755-1758

[6] ENTEROPATHOGENIC ESCHERICHIA-COLI DECREASES THE TRANSEPITHELIAL ELECTRICAL-RESISTANCE OF POLARIZED EPITHELIAL MONOLAYERS [J].

CANIL, C ;

ROSENSHINE, I ;

RUSCHKOWSKI, S ;

DONNENBERG, MS ;

KAPER, JB ;

FINLAY, BB .

INFECTION AND IMMUNITY, 1993, 61 (07) :2755-2762

[7] Rapid modulation of electrolyte transport in Caco-2 cell monolayers by enteropathogenic Escherichia coli (EPEC) infection [J].

Collington, GK ;

Booth, IW ;

Knutton, S .

GUT, 1998, 42 (02) :200-207

[8] The Yersinia Yop virulon: A bacterial system for subverting eukaryotic cells [J].

Cornelis, GR ;

WolfWatz, H .

MOLECULAR MICROBIOLOGY, 1997, 23 (05) :861-867

[9] Activation of host cell protein kinase C by enteropathogenic Escherichia coli [J].

Crane, JK ;

Oh, JS .

INFECTION AND IMMUNITY, 1997, 65 (08) :3277-3285

[10]

DYTOC M, 1994, GASTROENTEROLOGY, V106, P1105

← 1 2 3 4 →