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 journalArticle

    563 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

    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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  • Cite this

    Haegel, H., Larue, L., Ohsugi, M., Fedorov, L., Herrenknecht, K., & Kemler, R. (1995). Lack of β-catenin affects mouse development at gastrulation. Development, 121(11), 3529-3537.