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Figure from Pizarro-Cerda et al. Cell 2006

Invasive Molecular Strategies of Salmonella, Shigella, Yersinia and Listeria. (A) Salmonella translocates several effectors into target cells, several of them allowing the intial uptake of the bacterium: SipC is part of the TTSS and drives actin polymerization and actin-filament bundling; SopE activates Rho GTPases, fostering actin polimerization and membrane ruffle formation; SopB modulates inositol-polyphosphate metabolism, activating indirectly the same Rho GTPases as SopE; and SipA blocks the actin depolymerization factor cofilin, favoring also membrane ruffle formation. SptP plays a role once the internalization has taken place, inactivating the Rho GTPases, inhibiting actin polymerization and helping the closure of the plasma membrane over ineternalized bacteria. (B) Shigella also translocates several TTSS effectors into target cells to induce invasion: VirA indirectly stimulates the RhoGTPase Rac1 favoring actin polymerization (the host tyrosine kinases Abl/Arg also activate indirectly Cdc42 and Rac1) and inhibits microtubule polymerization; IpgD affects phosphoinositide metabolism and promotes the extension of membrane ruffles by decreasing the interactions between the plasma membrane and the actin cytoskeleton; IpaA activates the host protein vinculin, inducing actin depolymerization and recovery of the plasma membrane architecture once the bacteria are internalized. (C) The Yersinia outer membrane invasin interacts with b1 integrin receptors and favors activation of the small RhoGTPase Rac1, which will indirectly modulate the phosphatidylinositol metabolism to induce actin rearragements at the site of bacterial entry, promoting invasion. Host kinases such as FAK or Src also participate in the process.