Figure 1. Activation of Rho, Rac and Cdc42 controls actin polymerization during phagocytosis.

Figure 1

Activation of Rho, Rac and Cdc42 controls actin polymerization during phagocytosis. Left, a general model for phagocytic signalling. Phagocytosis generally involves the receptor-mediated, GEF-dependent activation of one or more Rho GTP-binding proteins, which will activate—through downstream effectors—the Arp2/3 complex and actin polymerisation. Several bacterial pathogens have the capacity to produce toxins or bacterial effectors (shown in double-lined boxes) that activate or inhibit the function or one or more Rho proteins, thereby modulating actin polymerization and phagocytosis. Right, the main signalling pathways activated during phagocytosis in mammalian cells. Type I phagocytosis is characterized by the independent activation of Rac and Cdc42, whereas only Rho activity is required during type II phagocytosis. GEF, guanine nucleotide exchange factor; CNF1, cytotoxic necrotizing factor 1 Tir, translocated intimin receptor; Yop, Yersinia outer protein; FcγR, Fcγ receptor; AC, apoptotic cell; CR3, complement receptor type 3; WASp, Wiskott-Aldrich Syndrome protein. See text for details.

From: Small GTP Binding Proteins and the Control of Phagocytic Uptake

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