HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Free via Open Access: OA OA Free Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Whale, A. D. Articles by Frankel, G. Search for Related Content PubMed PubMed Citation Articles by Whale, A. D. Articles by Frankel, G. Agricola Articles by Whale, A. D. Articles by Frankel, G.

TccP2-mediated subversion of actin dynamics by EPEC 2 – a distinct evolutionary lineage of enteropathogenic Escherichia coli

¹ Division of Cell and Molecular Biology, Imperial College London, London SW7 2AZ, UK
² Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal de São Paulo, São Paulo, Brazil
³ Division of Bioenvironmental Science, Frontier Science Research Center, University of Miyazaki, 5200 Kiyotake, Miyazaki 889-1692, Japan
⁴ Nationales Referenzlabor für Escherichia coli, Bundesinstitut für Risikobewertung, Diedersdorfer Weg 1, D-12277 Berlin, Germany
⁵ Centre for Paediatric Gastroenterology, Royal Free and University College Medical School, London, UK
⁶ Fundación Caubet-Cimera, Recinto Hospital Joan March, Carretera Soller Km 1207110 Bunyola, Mallorca, Spain

Correspondence
Gad Frankel
g.frankel{at}imperial.ac.uk

Enteropathogenic Escherichia coli (EPEC) is a major cause of infantile diarrhoea in developing countries. While colonizing the gut mucosa, EPEC triggers extensive actin-polymerization activity at the site of intimate bacterial attachment, which is mediated by avid interaction between the outer-membrane adhesin intimin and the type III secretion system (T3SS) effector Tir. The prevailing dogma is that actin polymerization by EPEC is achieved following tyrosine phosphorylation of Tir, recruitment of Nck and activation of neuronal Wiskott–Aldrich syndrome protein (N-WASP). In closely related enterohaemorrhagic E. coli (EHEC) O157 : H7, actin polymerization is triggered following recruitment of the T3SS effector TccP/EspF_U (instead of Nck) and local activation of N-WASP. In addition to tccP, typical EHEC O157 : H7 harbour a pseudogene (tccP2). However, it has recently been found that atypical, sorbitol-fermenting EHEC O157 carries functional tccP and tccP2 alleles. Interestingly, intact tccP2 has been identified in the incomplete genome sequence of the prototype EPEC strain B171 (serotype O111 : H–), but it is missing from another prototype EPEC strain E2348/69 (O127 : H7). E2348/69 and B171 belong to two distinct evolutionary lineages of EPEC, termed EPEC 1 and EPEC 2, respectively. Here, it is reported that while both EPEC 1 and EPEC 2 triggered actin polymerization via the Nck pathway, tccP2 was found in 26 of 27 (96.2 %) strains belonging to EPEC 2, and in none of the 34 strains belonging to EPEC 1. It was shown that TccP2 was: (i) translocated by the locus of enterocyte effacement-encoded T3SS; (ii) localized at the tip of the EPEC 2-induced actin-rich pedestals in infected HeLa cells and human intestinal in vitro organ cultures ex vivo; and (iii) essential for actin polymerization in infected Nck–/– cells. Therefore, unlike strains belonging to EPEC 1, strains belonging to EPEC 2 can trigger actin polymerization using both Nck and TccP2 actin-polymerization signalling cascades.

The GenBank/EMBL/DDBJ accession numbers for the sequences determined in this paper are AB271153 (O111 : H2 strain CB07077), AB271154 (O111 : H2 strain CB03447) and AB271155 (O111 : H2 strain CB03454).

This article has been cited by other articles:

				L. Bai, S. Schuller, A. Whale, A. Mousnier, O. Marches, L. Wang, T. Ooka, R. Heuschkel, F. Torrente, J. B. Kaper, et al. Enteropathogenic Escherichia coli O125:H6 Triggers Attaching and Effacing Lesions on Human Intestinal Biopsy Specimens Independently of Nck and TccP/TccP2 Infect. Immun., January 1, 2008; 76(1): 361 - 368. [Abstract] [Full Text] [PDF]