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Cytokines in immune regulation
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Published online 4 April 2005. doi:10.1083/jcb.200412162
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 169, Number 1, 139-149
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Article

 Phosphatidylinositol-4,5-bisphosphate hydrolysis directs actin remodeling during phagocytosis

Cameron C. Scott1,2, Wendy Dobson1, Roberto J. Botelho1,2, Natasha Coady-Osberg1, Philippe Chavrier3, David A. Knecht4, Colin Heath5, Philip Stahl5, and Sergio Grinstein1,2

1 Division of Cell Biology, The Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada
2 Department of Biochemistry, University of Toronto, Toronto, Ontario M5S 1A8, Canada
3 Membrane and Cytoskeleton Dynamics Group, UMR 144 Centre National de la Recherche Scientifique, Institut Curie, F-75248 Paris Cedex 05, France
4 Department of Molecular and Cell Biology, U-3125 University of Connecticut, Storrs, CT 06269
5 Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO 63110

Correspondence to Sergio Grinstein: sga{at}sickkids.ca

The Rho GTPases play a critical role in initiating actin polymerization during phagocytosis. In contrast, the factors directing the disassembly of F-actin required for fission of the phagocytic vacuole are ill defined. We used fluorescent chimeric proteins to monitor the dynamics of association of actin and active Cdc42 and Rac1 with the forming phagosome. Although actin was found to disappear from the base of the forming phagosome before sealing was complete, Rac1/Cdc42 activity persisted, suggesting that termination of GTPase activity is not the main determinant of actin disassembly. Furthermore, fully internalized phagosomes engineered to associate constitutively with active Rac1 showed little associated F-actin. The disappearance of phosphatidylinositol-4,5-bisphosphate (PI(4,5)P2) from the phagosomal membrane closely paralleled the course of actin disassembly. Furthermore, inhibition of PI(4,5)P2 hydrolysis or increased PI(4,5)P2 generation by overexpression of phosphatidylinositol phosphate kinase I prevented the actin disassembly necessary for the completion of phagocytosis. These observations suggest that hydrolysis of PI(4,5)P2 dictates the remodeling of actin necessary for completion of phagocytosis.

Abbreviations used in this paper: Fc{gamma}R, Fc{gamma} family of receptors; PIPKI, phosphatidylinositol phosphate kinase type I; PI(4,5)P2, phosphatidylinositol-4,5-bisphosphate; PBD-YFP, p21-binding domain of PAK fused to YFP; PI3-K, phosphatidylinositol 3'-kinase.


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