Integrin-dependent actomyosin contraction regulates epithelial cell scattering

被引:250
作者
de Rooij, J [1 ]
Kerstens, A
Danuser, G
Schwartz, MA
Waterman-Storer, CM
机构
[1] Scripps Res Inst, Dept Cell Biol, La Jolla, CA 92037 USA
[2] Univ Virginia, Mellon Prostate Canc Inst, Dept Microbiol, Cardiovasc Res Ctr, Charlottesville, VA 22908 USA
[3] Univ Virginia, Mellon Prostate Canc Inst, Dept Biomed Engn, Cardiovasc Res Ctr, Charlottesville, VA 22908 USA
关键词
D O I
10.1083/jcb.200506152
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The scattering of Madin-Darby canine kidney cells in vitro mimics key aspects of epithelial-mesenchymal transitions during development, carcinoma cell invasion, and metastasis. Scattering is induced by hepatocyte growth factor ( HGF) and is thought to involve disruption of cadherin-dependent cell-cell junctions. Scattering is enhanced on collagen and fibronectin, as compared with laminin1, suggesting possible cross talk between integrins and cell-cell junctions. We show that HGF does not trigger any detectable decrease in E-cadherin function, but increases integrin-mediated adhesion. Time-lapse imaging T suggests that tension on cell-cell junctions may disrupt cell-cell adhesion. Varying the density and type of extracellular matrix proteins shows that scattering correlates with stronger integrin adhesion and increased phosphorylation of the myosin regulatory light chain. To directly test the role of integrin-dependent traction forces, substrate compliance was varied. Rigid substrates that produce high traction forces promoted scattering, in comparison to more compliant substrates. We conclude that integrin-dependent actomyosin traction force mediates the disruption of cell-cell adhesion during epithelial cell scattering.
引用
收藏
页码:153 / 164
页数:12
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