Contact Inhibition of Locomotion in vivo controls neural crest directional migration
By Carlos Carmona-Fontaine, Helen K. Matthews, S. Kuriyama, Mauricio Moreno, G. Dunn, M. Parsons, C. Stern, Roberto Mayor. Nature, 2008
613 citations recorded by the source corpus.
Contact inhibition of locomotion was discovered by Abercrombie more than 50 years ago and describes the behaviour of fibroblast cells confronting each other in vitro, where they retract their protrusions and change direction on contact. Its failure was suggested to contribute to malignant invasion. However, the molecular basis of contact inhibition of locomotion and whether it also occurs in vivo are still unknown. Here we show that neural crest cells, a highly migratory and multipotent embryonic cell population, whose behaviour has been likened to malignant invasion, demonstrate contact inhibition of locomotion both in vivo and in vitro, and that this accounts for their directional migration. When two migrating neural crest cells meet, they stop, collapse their protrusions and change direction. In contrast, when a neural crest cell meets another cell type, it fails to display contact inhibition of locomotion; instead, it invades the other tissue, in the same manner as metastatic cancer cells. We show that inhibition of non-canonical Wnt signalling abolishes both contact inhibition of locomotion and the directionality of neural crest migration. Wnt-signalling members localize at the site of cell contact, leading to activation of RhoA in this region. These results provide the first example of contact inhibition of locomotion in vivo, provide an explanation for coherent directional migration of groups of cells and establish a previously unknown role for non-canonical Wnt signalling.
Subfields: Cell Biology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/b6adee2da34d3359dfc6da72e060cc1be49bae74
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Citations in the corpus
- Random versus directionally persistent cell migration (2009, background): “, which is partially responsible for the directional migration of neural crest cell”
- Non-muscle myosin II takes centre stage in cell adhesion and migration (2009, neutral): “RHOA activation, which activates NM II, also mediates contact inhibition of movement (that is, the inhibition of protrusion by cell–cell contact”
- Epithelial-mesenchymal transitions: the importance of changing cell state in development and disease. (2009, neutral): “Noncanonical Wnt signaling is also important for neural crest cell migration (65).”
- Epithelial-mesenchymal transitions in development and disease. (2009, background): “Elegant analyses at the single-cell resolution in Xenopus embryos have shown that contact inhibition of locomotion mediated by Wnt noncanonical signaling is a crucial mechanism for the directional movements of neural crest cells toward their target tissue (Carmona-Fontaine et al., 2008).”
- The ins and outs of the epithelial to mesenchymal transition in health and disease. (2011, background): “CIL has been recently verified in vivo during the migration of neural crest cells (Carmona-Fontaine et al. 2008).”
- A mechanically active heterotypic E-cadherin/N-cadherin adhesion enables fibroblasts to drive cancer cell invasion (2017, background): “Three classes of duration time were defined: longer than 60 min (>60), between 30 to 60 min (30-60) and less than 30 min (<30).”
- Collective cell migration in morphogenesis, regeneration and cancer (2009, background): “First, the cells remain physically and functionally connected such that the integrity of cell–cell junctions is preserved during movemen”
- Life at the leading edge. (2011, background): “Noncanonical Wnt signaling leads to activation of RhoA at sites of contact between neural crest cells, which then represses lamellipodia through its target ROCK (Carmona-Fontaine et al., 2008), presumably through increased actomyosin contractility.”