CUED Publications database

In vivo collective cell migration requires an LPAR2-dependent increase in tissue fluidity.

Kuriyama, S and Theveneau, E and Benedetto, A and Parsons, M and Tanaka, M and Charras, G and Kabla, A and Mayor, R (2014) In vivo collective cell migration requires an LPAR2-dependent increase in tissue fluidity. J Cell Biol, 206. pp. 113-127.

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Abstract

Collective cell migration (CCM) and epithelial-mesenchymal transition (EMT) are common to cancer and morphogenesis, and are often considered to be mutually exclusive in spite of the fact that many cancer and embryonic cells that have gone through EMT still cooperate to migrate collectively. Here we use neural crest (NC) cells to address the question of how cells that have down-regulated cell-cell adhesions can migrate collectively. NC cell dissociation relies on a qualitative and quantitative change of the cadherin repertoire. We found that the level of cell-cell adhesion is precisely regulated by internalization of N-cadherin downstream of lysophosphatidic acid (LPA) receptor 2. Rather than promoting the generation of single, fully mesenchymal cells, this reduction of membrane N-cadherin only triggers a partial mesenchymal phenotype. This intermediate phenotype is characterized by an increase in tissue fluidity akin to a solid-like-to-fluid-like transition. This change of plasticity allows cells to migrate under physical constraints without abolishing cell cooperation required for collectiveness.

Item Type: Article
Uncontrolled Keywords: Animals Cadherins Cell Adhesion Chemotaxis Intercellular Junctions Lysophospholipids Neural Crest Phosphorylation Protein Processing, Post-Translational Protein Transport Receptors, Lysophosphatidic Acid Signal Transduction Xenopus Proteins Xenopus laevis
Subjects: UNSPECIFIED
Divisions: Div C > Biomechanics
Depositing User: Cron Job
Date Deposited: 17 Jul 2017 18:58
Last Modified: 23 Nov 2017 03:35
DOI: