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Published online December 10, 2007
doi:10.1083/jcb.200708093
The Journal of Cell Biology, Vol. 179, No. 6, 1275-1287
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Owen et al.
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Article

 Regulation of lamellipodial persistence, adhesion turnover, and motility in macrophages by focal adhesion kinase

Katherine A. Owen1, Fiona J. Pixley3, Keena S. Thomas1, Miguel Vicente-Manzanares2, Brianne J. Ray1, Alan F. Horwitz2, J. Thomas Parsons1, Hilary E. Beggs4, E. Richard Stanley5, and Amy H. Bouton1

1 Department of Microbiology and 2 Department of Cell Biology, University of Virginia Health System, Charlottesville, VA 22908
3 Pharmacology and Anaesthesiology Unit, School of Medicine and Pharmacology, Queen Elizabeth II Medical Centre, Nedlands, WA 6009, Australia
4 Department of Ophthalmology, University of California, San Francisco, San Francisco, CA 94143
5 Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY 10461

Correspondence to Amy H. Bouton: ahb8y{at}virginia.edu

Macrophages are a key component of the innate immune system. In this study, we investigate how focal adhesion kinase (FAK) and the related kinase Pyk2 integrate adhesion signaling and growth factor receptor signaling to regulate diverse macrophage functions. Primary bone marrow macrophages isolated from mice in which FAK is conditionally deleted from cells of the myeloid lineage exhibited elevated protrusive activity, altered adhesion dynamics, impaired chemotaxis, elevated basal Rac1 activity, and a marked inability to form stable lamellipodia necessary for directional locomotion. The contribution of FAK to macrophage function in vitro was substantiated in vivo by the finding that recruitment of monocytes to sites of inflammation was impaired in the absence of FAK. Decreased Pyk2 expression in primary macrophages also resulted in a diminution of invasive capacity. However, the combined loss of FAK and Pyk2 had no greater effect than the loss of either molecule alone, indicating that both kinases function within the same pathway to promote invasion.

Abbreviations used in this paper: BMM, bone marrow macrophage; CSF-1, colony-stimulating factor-1; FN, fibronectin; LysM, lysozyme M; MCP-1, macrophage chemoattractant protein-1; PE, phycoerythrin; SDF-1{alpha}, stromal cell–derived factor-1{alpha}; TG, thioglycollate; TIRF, total internal reflective fluorescence; WT, wild type.


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