NCK1 and infection: In a similar manner to tccP-positive EPEC and EHEC strains, but in contrast to prototypical EPEC 1 strains, B171 was able to efficiently trigger Nck-independent actin polymerization, an activity dependent on tccP2. Due to the high level of sequence conservation between TccP and TccP2, we observed functional redundancy between the two TccP homologues: TccP2 was able to restore actin-polymerization ability to EDL933ΔtccP during infection of HeLa cells, and TccP was able to complement B171ΔtccP2 for triggering actin remodelling during infection of Nck1−/Nck2− fibroblasts.