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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引用

Bass, M. D., Roach, K. A., Morgan, M. R., Mostafavi-Pour, Z., Schoen, T., Muramatsu, T., Mayer, U., Ballestrem, C., Spatz, J. P., & Humphries, M. J. (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.

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

要旨

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.