Colonization of the intestinal mucosa by enteropathogenic and enterohaemorrhagic E. coli (EPEC and EHEC) can lead to acute and chronic diarrhoea and, in the case of EHEC, to renal and neurological complications. These pathogens usurp the host cell cytoskeleton both by destruction of the microvilli brush border and by re-directing actin filament assembly below contact sites with the host cell plasma membrane, driving the formation of characteristic pseudopodia, socalled pedestals on which these bacteria reside. The resulting „attaching and effacing“ (A/E) phenotype of the intestinal epithelium is thought to contribute to the development of disease, although the exact mechanisms are unknown. Molecular analyses of these processes had implicated the involvement of numerous cytoskeletal proteins in pedestal formation, such as the prominent actin filament nucleation promoting factor N-WASP. The generation and characterization of N-WASP-defective cells lines from a conditional N-WASP knockout mouse was prerequisite to establishing that this protein is essential for pedestal formation induced by both EPEC and EHEC. Infections with these pathogens of knockout cell lines, but not of their parental precursors, caused a complete abolishment of pedestal formation, while ectopic re-expression of EGFP-tagged N-WASP in N-WASP null cells fully restored this type of actin reorganization. Thus, the absence of actin assembly in these cells can solely be explained by loss of N-WASP function. Therefore, these cells constitute an excellent tool for further dissection of the molecular pathways leading to recruitment and activation of N-WASP at the contact site between EPEC or EHEC and the host cell surface. As opposed to these pathogenic E. coli , which remain on the host cell exterior, some enteric pathogens have evolved to induce their own phagocytosis, again an actin-dependent process, leading to epithelial cell invasion, dissemination within the epithelium or beyond. Together, we therefore propose here to analyse the molecular regulation of these distinct types of actin reorganization induced by different bacterial pathogens when encountering the intestinal epithelium.