Integrin-dependent actomyosin contraction regulates epithelial cell scattering

Johan De Rooij, Andre Kerstens, Gaudenz Danuser, Martin A. Schwartz, Clare M. Waterman-Storer

Research output: Contribution to journalArticle

226 Scopus citations

Abstract

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 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 integrindependent actomyosin traction force mediates the disruption of cell-cell adhesion during epithelial cell scattering.

Original languageEnglish (US)
Pages (from-to)153-164
Number of pages12
JournalJournal of Cell Biology
Volume171
Issue number1
DOIs
StatePublished - Oct 2005

ASJC Scopus subject areas

  • Cell Biology

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