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Dev Biol October 15, 2014; 394 (2): 340-56.

FAK is required for tension-dependent organization of collective cell movements in Xenopus mesendoderm.

Bjerke MA , Dzamba BJ , Wang C , DeSimone DW .

Collective cell movements are integral to biological processes such as embryonic development and wound healing and also have a prominent role in some metastatic cancers. In migrating Xenopus mesendoderm, traction forces are generated by cells through integrin-based adhesions and tension transmitted across cadherin adhesions. This is accompanied by assembly of a mechanoresponsive cadherin adhesion complex containing keratin intermediate filaments and the catenin-family member plakoglobin. We demonstrate that focal adhesion kinase (FAK), a major component of integrin adhesion complexes, is required for normal morphogenesis at gastrulation, closure of the anterior neural tube, axial elongation and somitogenesis. Depletion of zygotically expressed FAK results in disruption of mesendoderm tissue polarity similar to that observed when expression of keratin or plakoglobin is inhibited. Both individual and collective migrations of mesendoderm cells from FAK depleted embryos are slowed, cell protrusions are disordered, and cell spreading and traction forces are decreased. Additionally, keratin filaments fail to organize at the rear of cells in the tissue and association of plakoglobin with cadherin is diminished. These findings suggest that FAK is required for the tension-dependent assembly of the cadherin adhesion complex that guides collective mesendoderm migration, perhaps by modulating the dynamic balance of substrate traction forces and cell cohesion needed to establish cell polarity.

PubMed ID: 25127991
PMC ID: PMC4172504
Article link: Dev Biol
Grant support: [+]

Species referenced: Xenopus
Genes referenced: ctnnb1 fn1 jup krt8.1 mapt ptk2
Antibodies: Fn1 Ab1
Morpholinos: ptk2 MO5

Article Images: [+] show captions
References [+] :
Beningo, Traction forces of fibroblasts are regulated by the Rho-dependent kinase but not by the myosin light chain kinase. 2006, Pubmed