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Molecular and Cellular Biology, September 2000, p. 6354-6363, Vol. 20, No. 17
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Coupling of PAK-Interacting Exchange Factor PIX to GIT1 Promotes Focal Complex Disassembly

Zhou-shen Zhao,1 Edward Manser,1,* Tsui-Han Loo,1 and Louis Lim1,2

Glaxo-IMCB Group, Institute of Molecular and Cell Biology, Singapore 117609, Singapore,1 and Institute of Neurology, London WC1N 1PJ, United Kingdom2

Received 7 February 2000/Returned for modification 11 April 2000/Accepted 24 May 2000

The p21-activated kinase PAK is targeted to focal complexes (FCs) through interactions with the SH3 domains of the PAK-interacting exchange factor PIX and Nck. PIX is a Rac GTP exchange factor that also binds the G-protein-coupled receptor kinase-interacting protein known as GIT1. Overexpression of GIT1 in fibroblasts or epithelial cells causes a loss of paxillin from FCs and stimulates cell motility. This is due to the direct interaction of a C-terminal 125-residue domain of GIT1 with paxillin, under the regulation of PIX. In its activated state, GIT1 can promote FC disassembly independent of actin-myosin contractile events. Additionally, GIT directly couples to a key component of FCs, focal adhesion kinase (FAK), via a conserved Spa2 homology domain. We propose that GIT1 and FAK cooperate to promote motility both by directly regulating focal complex dynamics and by the activation of Rac.

* Corresponding author. Mailing address: Glaxo-IMCB Group, Institute of Molecular & Cell Biology, 30 Medical Dr., Singapore 117609, Singapore. Phone: (65) 874-6167. Fax: (65) 774-0742. E-mail: mcbmansr{at}imcb.nus.edu.sg.

Molecular and Cellular Biology, September 2000, p. 6354-6363, Vol. 20, No. 17
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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