| First Author | Haegel H | Year | 1995 |
| Journal | Development | Volume | 121 |
| Issue | 11 | Pages | 3529-37 |
| PubMed ID | 8582267 | Mgi Jnum | J:29881 |
| Mgi Id | MGI:77405 | Doi | 10.1242/dev.121.11.3529 |
| Citation | Haegel H, et al. (1995) Lack of beta-catenin affects mouse development at gastrulation. Development 121(11):3529-37 |
| abstractText | Molecular analysis of the cadherin-catenin complex elucidated the central role of beta-catenin in this adhesion complex, as it binds to the cytoplasmic domain of E-cadherin and to alpha-catenin. beta-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 beta-catenin during mouse development, gene knock-out experiments were performed in embryonic stem cells and transgenic mice were generated. beta-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 beta-catenin is expressed rather ubiquitously, it is specifically required in the ectodermal cell layer. |
