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Infection and Immunity, September 2003, p. 4908-4916, Vol. 71, No. 9
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.9.4908-4916.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Contribution of the Twin Arginine Translocation System to the Virulence of Enterohemorrhagic Escherichia coli O157:H7

Laboratoire de Chimie Bactérienne, UPR9043, IBSM, CNRS, F-13402 Marseille Cedex 20,¹ Groupe de Recherche Pathogénie Bactérienne Intestinale, Université d'Auvergne Clermont-1, 63000 Clermont-Ferrand, France,³ Department of Diarrheal Diseases, National Institute of Communicable Diseases Prevention and Control, Chinese Center for Disease Control and Prevention, Beijing 102206, Peoples' Republic of China²

Received 5 March 2003/ Returned for modification 30 May 2003/ Accepted 17 June 2003

Shiga toxin-producing Escherichia coli O157:H7 is a major food-borne infectious pathogen. In order to analyze the contribution of the twin arginine translocation (TAT) system to the virulence of E. coli O157:H7, we deleted the tatABC genes of the O157:H7 EDL933 reference strain. The mutant displayed attenuated toxicity on Vero cells and completely lost motility on soft agar plates. Further analyses revealed that the tatABC mutation impaired the secretion of the Shiga toxin 1 (Stx1) and abolished the synthesis of H7 flagellin, which are two major known virulence factors of enterohemorrhagic E. coli O157:H7. Expression of the EDL933 stxAB₁ genes in E. coli K-12 conferred verotoxicity on this nonpathogenic strain. Remarkably, cytotoxicity assay and immunoblot analysis showed, for the first time, an accumulation of the holotoxin complex in the periplasm of the wild-type strain and that a much smaller amount of StxA₁ and reduced verotoxicity were detected in the tatC mutant cells. Together, these results establish that the TAT system of E. coli O157:H7 is an important virulence determinant of this enterohemorrhagic pathogen.

Editor: J. T. Barbieri

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