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XB-ART-49726
J Cell Biol July 7, 2014; 206 (1): 113-27.

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

Kuriyama S , Theveneau E , Benedetto A , Parsons M , Tanaka M , Charras G , Kabla A , Mayor R .


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.

PubMed ID: 25002680
PMC ID: PMC4085712
Article link: J Cell Biol
Grant support: [+]

Species referenced: Xenopus laevis
Genes referenced: cdh2 ctnnb1 ctnnd1 dlx2 enpp2 fli1 foxd3 gnl3 itk lpar1 lpar2 pxn rab5a rdx snai2 twist1 vcl wnt8a
Antibodies: Cdh2 Ab3 Ctnnb1 Ab5 Vcl Ab1
Morpholinos: enpp2 MO1 lpar1 MO2 lpar2 MO2


Article Images: [+] show captions
References [+] :
Alfandari, Mechanism of Xenopus cranial neural crest cell migration. 2010, Pubmed, Xenbase