Cadherin Switch during EMT in Neural Crest Cells Leads to Contact Inhibition of Locomotion via Repolarization of Forces

Dev Cell. 2015 Aug 24;34(4):421-34. doi: 10.1016/j.devcel.2015.06.012. Epub 2015 Jul 30.


Contact inhibition of locomotion (CIL) is the process through which cells move away from each other after cell-cell contact, and it contributes to malignant invasion and developmental migration. Various cell types exhibit CIL, whereas others remain in contact after collision and may form stable junctions. To investigate what determines this differential behavior, we study neural crest cells, a migratory stem cell population whose invasiveness has been likened to cancer metastasis. By comparing pre-migratory and migratory neural crest cells, we show that the switch from E- to N-cadherin during EMT is essential for acquisition of CIL behavior. Loss of E-cadherin leads to repolarization of protrusions, via p120 and Rac1, resulting in a redistribution of forces from intercellular tension to cell-matrix adhesions, which break down the cadherin junction. These data provide insight into the balance of physical forces that contributes to CIL in cells in vivo.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biomechanical Phenomena
  • Cadherins / metabolism*
  • Catenins / metabolism
  • Cell Movement*
  • Cell Polarity*
  • Contact Inhibition*
  • Epithelial-Mesenchymal Transition*
  • Intercellular Junctions / metabolism
  • Neural Crest / cytology*
  • Protein Binding
  • Xenopus laevis
  • rac1 GTP-Binding Protein / metabolism


  • Cadherins
  • Catenins
  • delta catenin
  • rac1 GTP-Binding Protein