Syndecan-4-dependent Rac1 regulation determines directional migration in 
response to the extracellular matrix

Bass, Mark D.; Roach, Kirsty A.; Morgan, Mark R.; Mostafavi-Pour, Zohreh; Schoen, Tobias; Muramatsu, Takashi; Mayer, Ulrike; Ballestrem, Christoph; Spatz, Joachim P.; Humphries, Martin J.

doi:10.1083/jcb.200610076

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Syndecan-4-dependent Rac1 regulation determines directional migration in response to the extracellular matrix

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Spatz, Joachim P.
Cellular Biophysics, Max Planck Institute for Medical Research, Max Planck Society;
Biophysical Chemistry, Institute of Physical Chemistry, University of Heidelberg, 69120 Heidelberg, Germany;

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Citation

Bass, M. D., Roach, K. A., Morgan, M. R., Mostafavi-Pour, Z., Schoen, T., Muramatsu, T., et al. (2007). Syndecan-4-dependent Rac1 regulation determines directional migration in response to the extracellular matrix. The Journal of Cell Biology: JCB, 177(3), 527-538. doi:10.1083/jcb.200610076.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0010-43A7-6

Abstract

Cell migration in wound healing and disease is critically dependent on integration with the extracellular matrix, but the receptors that couple matrix topography to migratory behavior remain obscure. Using nano-engineered fibronectin surfaces and cell-derived matrices, we identify syndecan-4 as a key signaling receptor determining directional migration. In wild-type fibroblasts, syndecan-4 mediates the matrix-induced protein kinase Calpha (PKCalpha)-dependent activation of Rac1 and localizes Rac1 activity and membrane protrusion to the leading edge of the cell, resulting in persistent migration. In contrast, syndecan-4-null fibroblasts migrate randomly as a result of high delocalized Rac1 activity, whereas cells expressing a syndecan-4 cytodomain mutant deficient in PKCalpha regulation fail to localize active Rac1 to points of matrix engagement and consequently fail to recognize and respond to topographical changes in the matrix.