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doi: 10.1242/10.1242/jcs.00605

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Coupling membrane protrusion and cell adhesion

Department of Cell and Developmental Biology and Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA

View larger version (24K): [in a new window]   Fig. 1. Integrin-mediated activation of the Arp2/3 complex. Left, in the absence of integrin engagement or other stimuli, Rac and Cdc42 are held in an inactive GDP-bound state. WAVE-1 exists in an inactive, heterotetrameric complex with HSPC, NAP125 and PIR. Right, integrin ligation triggers the exchange of GDP for GTP. Cdc42 binds and induces a conformational change in WASP that permits it to bind and activate the Arp2/3 complex. Rac and NCK disrupt the WAVE complex, causing it to disassemble and release WAVE in association with HSPC300. WAVE binds and activates the Arp2/3 complex.

View larger version (31K): [in a new window]   Fig. 2. Physical coupling of adhesion molecules to the actin polymerization machinery. Left, the Arp2/3 complex is directly recruited to sites of integrin engagement through an interaction with the linker region of vinculin, an integrin-associated protein. Right, the Arp2/3 complex is recruited to sites of cell-cell adhesion through an interaction with E-cadherin. Recruitment of the Arp2/3 complex to E-cadherin is thought to localize actin polymerization to sites of cadherin-engagement.

View larger version (42K): [in a new window]   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.