Fig. 3. Various bacterial pathogens and their mechanisms for stimulating membrane protrusion. Listeria monocytogenes adheres to host cells via the binding of a bacterial surface protein, internalin A (IlnA) to E-cadherin. E-cadherin, via Rac activation, can trigger dynamic events of actin polymerization and membrane extension, culminating in bacterial uptake. Yersinia expresses invasin on its surface, which binds with high affinity to 5ß1 integrins. Yersinia uptake requires Rac1 and the Arp2/3 complex. EPEC attach to host cells through translocated intimin receptor (TIR), a receptor secreted by EPEC and inserted into the host cell plasma membrane where it acts as a receptor for intimin. WASP and the Arp2/3 complex are recruited to sites of attachment and stimulate actin polymerization required for pedestal formation.