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Infection and Immunity, October 2008, p. 4669-4676, Vol. 76, No. 10
0019-9567/08/$08.00+0     doi:10.1128/IAI.00140-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Cortactin Recruitment by Enterohemorrhagic Escherichia coli O157:H7 during Infection In Vitro and Ex Vivo{triangledown}

Aurelie Mousnier,1,{dagger} Andrew D. Whale,1,{dagger} Stephanie Schüller,2 John M. Leong,3 Alan D. Phillips,2 and Gad Frankel1*

Division of Cell and Molecular Biology, Imperial College London,1 Centre for Paediatric Gastroenterology, Royal Free and University College Medical School, London, United Kingdom,2 Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester, Massachusetts3

Received 31 January 2008/ Returned for modification 7 March 2008/ Accepted 21 July 2008

Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is an important human pathogen that colonizes the gut mucosa via attaching and effacing (A/E) lesions; A/E lesion formation in vivo and ex vivo is dependent on the type III secretion system (T3SS) effector Tir. Infection of cultured cells by EHEC leads to induction of localized actin polymerization, which is dependent on Tir and a second T3SS effector protein, TccP, also known as EspFU. Recently, cortactin was shown to bind both the N terminus of Tir and TccP via its SH3 domain and to play a role in EHEC-triggered actin polymerization in vitro. In this study, we investigated the recruitment of cortactin to the site of EHEC adhesion during infection of in vitro-cultured cells and mucosal surfaces ex vivo (using human terminal ileal in vitro organ cultures [IVOC]). We have shown that cortactin is recruited to the site of EHEC adhesion in vitro downstream of TccP and N-WASP. Deletion of the entire N terminus of Tir or replacing the N-terminal polyproline region with alanines did not abrogate actin polymerization or cortactin recruitment. In contrast, recruitment of cortactin to the site of EHEC adhesion in IVOC is TccP independent. These results imply that cortactin is recruited to the site of EHEC adhesion in vitro and ex vivo by different mechanisms and suggest that cortactin might have a role during EHEC infection of mucosal surfaces.

* Corresponding author. Mailing address: Division of Molecular and Cellular Biology, Flowers Building, Imperial College London, London SW7 2AZ, United Kingdom. Phone: 44 020 2594 5253. Fax: 44 020 5794 3069. E-mail: g.frankel{at}imperial.ac.uk

{triangledown} Published ahead of print on 4 August 2008.

Editor: J. B. Bliska

{dagger} A.M. and A.D.W. contributed equally to this work.

Infection and Immunity, October 2008, p. 4669-4676, Vol. 76, No. 10
0019-9567/08/$08.00+0     doi:10.1128/IAI.00140-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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