Letter abstract
Nature Cell Biology 6, 154 - 161 (2004)
Published online: 25 January 2004 | doi:10.1038/ncb1094
FAK–Src signalling through paxillin, ERK and MLCK regulates adhesion disassembly
Donna J. Webb1, Karen Donais1, Leanna A. Whitmore1, Sheila M. Thomas3, Christopher E. Turner4, J. Thomas Parsons2 & Alan F. Horwitz1
Cell migration is a complex, highly regulated process that involves the continuous formation and disassembly of adhesions (adhesion turnover). Adhesion formation takes place at the leading edge of protrusions, whereas disassembly occurs both at the cell rear and at the base of protrusions. Despite the importance of these processes in migration, the mechanisms that regulate adhesion formation and disassembly remain largely unknown. Here we develop quantitative assays to measure the rate of incorporation of molecules into adhesions and the departure of these proteins from adhesions. Using these assays, we show that kinases and adaptor molecules, including focal adhesion kinase (FAK), Src, p130CAS, paxillin, extracellular signal-regulated kinase (ERK) and myosin light-chain kinase (MLCK) are critical for adhesion turnover at the cell front, a process central to migration.
- Department of Cell Biology, UVA School of Medicine, P.O. Box 800732, Charlottesville, Virginia 22908-0732, USA.
- Department of Microbiology, University of Virginia, Charlottesville, VA 22908, USA.
- Cancer Biology Program, Harvard Medical School, Boston, MA 02215, USA.
- Department of Cell and Developmental Biology, SUNY Upstate Medical University, Syracuse, NY 13210, USA.
Correspondence to: Donna J. Webb1 e-mail: djw2p@virginia.edu
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