| First Author | Junghans D | Year | 2005 |
| Journal | Dev Dyn | Volume | 233 |
| Issue | 2 | Pages | 528-39 |
| PubMed ID | 15844200 | Mgi Jnum | J:129254 |
| Mgi Id | MGI:3768946 | Doi | 10.1002/dvdy.20365 |
| Citation | Junghans D, et al. (2005) Beta-catenin-mediated cell-adhesion is vital for embryonic forebrain development. Dev Dyn 233(2):528-39 |
| abstractText | Forming a complex structure such as the mammalian brain requires a complex interplay between cells and different signalling cascades during embryonic development. beta-catenin plays pivotal roles in these processes by mediating cadherin-based cell adhesion and Wnt signalling. We show for the first time that beta-catenin functions predominantly as a mediator of cell adhesion during early development of the mammalian telencephalon. Immunohistochemical analysis demonstrates that beta-catenin is localized, together with N-cadherin, to adhesion junctions at the apical lining of the neuroepithelium. The ablation of beta-catenin specifically from the forebrain leads to a disruption of apical adherens junctions and a breakdown of neuroepithelial structures. We show that beta-catenin-deficient neuroepithelial cells delaminate and undergo apoptosis. Newborn beta-catenin mutants lack the entire forebrain and anterior facial structures. Our data also indicate a lack of TCF/LEF-beta-catenin-dependent transcriptional activity in the telencephalon of Wnt reporter embryos. Together with the absence of nuclear beta-catenin, this finding suggests that canonical Wnt signalling is not active during early telencephalic development. In summary, we demonstrate that beta-catenin mediates cell-cell adhesion in the early telencephalon and is vital for maintaining the structural integrity of the neuroepithelium. |
