Lack of β-catenin affects mouse development at gastrulation

H. Haegel, L. Larue, M. Ohsugi, L. Fedorov, K. Herrenknecht, R. Kemler

Research output: Contribution to journalArticlepeer-review

569 Scopus citations

Abstract

Molecular analysis of the cadherin-catenin complex elucidated the central role of β-catenin in this adhesion complex, as it binds to the cytoplasmic domain of E-cadherin and to α-catenin. β-catenin may also function in signalling pathways, given its homology to the gene product of the Drosophila segment polarity gene armadillo, which is known to be involved in the wingless signalling cascade. To study the function of β-catenin during mouse development, gene knock-out experiments were performed in embryonic stem cells and transgenic mice were generated. β-catenin null-mutant embryos formed blastocysts, implanted and developed into egg-cylinder-stage embryos. At day 7 post coitum, the development of the embryonic ectoderm was affected in mutant embryos. Cells detached from the ectodermal cell layer and were dispersed into the proamniotic cavity. No mesoderm formation was observed in mutant embryos. The development of extraembryonic structures appeared less dramatically or not at all affected. Our results demonstrate that, although β-catenin is expressed rather ubiquitously, it is specifically required in the ectodermal cell layer.

Original languageEnglish (US)
Pages (from-to)3529-3537
Number of pages9
JournalDevelopment
Volume121
Issue number11
StatePublished - Jan 1 1995
Externally publishedYes

Keywords

  • Cell adhesion
  • E-cadherin
  • Embryonic stem cells
  • Knock-out mutant
  • Mouse embryogenesis
  • β-catenin

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology

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