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Vol. 20, Issue 9, 2508-2519, May 1, 2009

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Focal Adhesion Kinase Modulates Cell Adhesion Strengthening via Integrin Activation

Kristin E. Michael^*, David W. Dumbauld^*, Kellie L. Burns^*, Steven K. Hanks, and Andrés J. García^*

*Woodruff School of Mechanical Engineering and Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, GA 30332; and Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN 37232

Submitted January 24, 2008; Revised March 6, 2009; Accepted March 9, 2009
Monitoring Editor: Martin A. Schwartz

Focal adhesion kinase (FAK) is an essential nonreceptor tyrosine kinase regulating cell migration, adhesive signaling, and mechanosensing. Using FAK-null cells expressing FAK under an inducible promoter, we demonstrate that FAK regulates the time-dependent generation of adhesive forces. During the early stages of adhesion, FAK expression in FAK-null cells enhances integrin activation to promote integrin binding and, hence, the adhesion strengthening rate. Importantly, FAK expression regulated integrin activation, and talin was required for the FAK-dependent effects. A role for FAK in integrin activation was confirmed in human fibroblasts with knocked-down FAK expression. The FAK autophosphorylation Y397 site was required for the enhancements in adhesion strengthening and integrin-binding responses. This work demonstrates a novel role for FAK in integrin activation and the time-dependent generation of cell–ECM forces.

Address correspondence to: Andrés J. García (andres.garcia{at}me.gatech.edu)

Abbreviations used: FAK, focal adhesion kinase.

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