Embryonic mesodermal defects in α5 integrin-deficient mice

Joy T. Yang, Helen Rayburn, Richard O. Hynes

Research output: Contribution to journalArticlepeer-review

585 Scopus citations


A loss of function mutation of the murine α5 integrin gene generated by gene targeting in embryonic stem cells is a recessive embryonic lethal. The mutant embryos start to show observable defects by day 9 of gestation and die around day 10-11. The α5-null embryos have pronounced defects in posterior trunk and yolk sac mesodermal structures, suggesting a role for α5β1 integrin in mesoderm formation, movement or function. However, the embryos progress significantly further than embryos null for fibronectin, for which α5β1 integrin is a receptor, suggesting the involvement of other fibronectin receptors. In vitro studies on cells derived from the α5-null embryos confirm that the α5β1 integrin is not expressed on mutant cells and show that the mutant cells are able to assemble fibronectin matrix, form focal contacts, and migrate on fibronectin despite the complete absence of the α5β1 fibronectin receptor integrin. All these functions have previously been thought to involve or require α5β1. The results presented show that these cellular functions involving fibronectin can proceed using other receptors.

Original languageEnglish (US)
Pages (from-to)1093-1105
Number of pages13
Issue number4
StatePublished - Dec 1993
Externally publishedYes


  • α integrin
  • Embryonic stem cell
  • Fibronectin

ASJC Scopus subject areas

  • Cell Biology
  • Anatomy


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