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. 2009 Jan 26;184(2):281–296. doi: 10.1083/jcb.200806121

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© 2009 Mao et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 9. — Model for the unique roles and differential regulations of PIP5K-γ and -α in FcγR-mediated phagocytosis. Controlled actin depolymerization is initiated upon FcγR ligation to IgG. PIP5K-γ activates Rac and inhibits Rho, tilting the balance toward actin disassembly. Actin remodeling releases the “tethering” of FcγR to promote formation of FcγR microclusters, which promote particle binding and downstream signaling including ERK and Syk activation. Syk further phosphorylates and activates PIP5K-γ in a positive feed-forward manner. PIP5K-α generates PIP₂ at the nascent phagocytic cup to activate WASP family proteins. Arp2/3 binds activated WASP and initiates de novo actin polymerization for particle ingestion. Our model places PIP5K-γ upstream of Rac/Rho based on data presented here, and places PIP5K-α downstream of Rac/Cdc42 based on previous published results and PIP5K-α's role in WASP activation described here. Our model does not preclude additional feedback regulation of PIP5K-γ by these small GTPases.