Journal
DEVELOPMENTAL CELL
Volume 34, Issue 4, Pages 421-434Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2015.06.012
Keywords
-
Categories
Funding
- MRC [M010465, J000655]
- BBSRC [M008517]
- Wellcome Trust
- Wellcome Trust Value in People Award (UCL)
- CNRS
- Fondation pour la Recherche Medicale [AJE201224]
- Midi-Pyrenees Regional Council
- EMBO
- European Union [329968]
- BBSRC [BB/M008517/1] Funding Source: UKRI
- MRC [MR/M010465/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/M008517/1] Funding Source: researchfish
- Medical Research Council [MR/M010465/1] Funding Source: researchfish
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available