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Published 19 July 2004. doi:10.1083/jcb.200402073
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 166, Number 2, 225-235
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Article

 Cortactin and Crk cooperate to trigger actin polymerization during Shigella invasion of epithelial cells

Laurence Bougnères1, Stéphane E. Girardin1, Scott A. Weed3, Andrei V. Karginov4, Jean-Christophe Olivo-Marin2, J. Thomas Parsons4, Philippe J. Sansonetti1, and Guy Tran Van Nhieu1

1 Unité de Pathogénie Microbienne Moléculaire, INSERM U389
2 Unité d'Analyse d'Images Quantitative, Institut Pasteur, 75724 Paris Cedex 15, France
3 Department of Craniofacial Biology, University of Colorado Health Sciences Center, Denver, CO 80262
4 Department of Microbiology Health Sciences Center, University of Virginia, Charlottesville, VA 22908

Address correspondence to G. Tran Van Nhieu, Unité de Pathogénie Microbienne Moléculaire, INSERM U389, Institut Pasteur, 28 rue du Dr. Roux, 75724 Paris Cedex 15, France. Tel.: (33) 1-45-68-83-15. Fax: (33) 1-45-68-89-53. email: gtranvan{at}pasteur.fr

Shigella, the causative agent of bacillary dysentery, invades epithelial cells in a process involving Src tyrosine kinase signaling. Cortactin, a ubiquitous actin-binding protein present in structures of dynamic actin assembly, is the major protein tyrosine phosphorylated during Shigella invasion. Here, we report that RNA interference silencing of cortactin expression, as does Src inhibition in cells expressing kinase-inactive Src, interferes with actin polymerization required for the formation of cellular extensions engulfing the bacteria. Shigella invasion induced the recruitment of cortactin at plasma membranes in a tyrosine phosphorylation–dependent manner. Overexpression of wild-type forms of cortactin or the adaptor protein Crk favored Shigella uptake, and Arp2/3 binding–deficient cortactin derivatives or an Src homology 2 domain Crk mutant interfered with bacterial-induced actin foci formation. Crk was shown to directly interact with tyrosine-phosphorylated cortactin and to condition cortactin-dependent actin polymerization required for Shigella uptake. These results point at a major role for a Crk–cortactin complex in actin polymerization downstream of tyrosine kinase signaling.

Key Words: Shigella; invasion; cortactin; Crk; actin

Abbreviations used in this paper: FL, full-length; p130Cas, p130 Crk-associated substrate; SH, Src homology; TM, tyrosine-mutated.


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