| First Author | He F | Year | 2010 |
| Journal | Dev Dyn | Volume | 239 |
| Issue | 12 | Pages | 3235-46 |
| PubMed ID | 20981831 | Mgi Jnum | J:166721 |
| Mgi Id | MGI:4849351 | Doi | 10.1002/dvdy.22466 |
| Citation | He F, et al. (2010) Gsk3beta is required in the epithelium for palatal elevation in mice. Dev Dyn 239(12):3235-46 |
| abstractText | In Wnt/beta-catenin signaling pathway, Gsk3beta functions to facilitate beta-catenin degradation. Inactivation of Gsk3beta in mice causes a cleft palate formation, suggesting an involvement of Wnt/beta-catenin signaling during palatogenesis. In this study, we have investigated the expression pattern, tissue-specific requirement and function of Gsk3beta during mouse palatogenesis. We showed that Gsk3beta is primarily expressed in the palatal epithelium, particularly in the medial edge epithelium overlapping with beta-catenin. Tissue-specific gene inactivation studies demonstrated an essential role for Gsk3beta in the epithelium for palate elevation, and disruption of which contributes to cleft palate phenotype in Gsk3beta mutant. We observed that expression of Aixn2, a direct target gene of Wnt/beta-catenin signaling, is ectopically activated in the mutant tongue, but not in the palate. Our results indicate that Gsk3beta is an intrinsic regulator required in the epithelium for palate elevation, and could act through a pathway independent of Wnt/beta-catenin signaling to regulate palate development. |
