| First Author | Gu S | Year | 2008 |
| Journal | Dev Dyn | Volume | 237 |
| Issue | 5 | Pages | 1509-16 |
| PubMed ID | 18393307 | Mgi Jnum | J:134348 |
| Mgi Id | MGI:3785349 | Doi | 10.1002/dvdy.21534 |
| Citation | Gu S, et al. (2008) Mice with an anterior cleft of the palate survive neonatal lethality. Dev Dyn 237(5):1509-16 |
| abstractText | Many genes are known to function in a region-specific manner in the developing secondary palate. We have previously shown that Shox2-deficient embryos die at mid-gestation stage and develop an anterior clefting phenotype. Here, we show that mice carrying a conditional inactivation of Shox2 in the palatal mesenchyme survive the embryonic and neonatal lethality, but develop a wasting syndrome. Phenotypic analyses indicate a delayed closure of the secondary palate at the anterior end, leading to a failed fusion of the primary and secondary palates. Consistent with a role proposed for Shox2 in skeletogenesis, Shox2 inactivation causes a significantly reduced bone formation in the hard palate, probably due to a down-regulation of Runx2 and Osterix. We conclude that the secondary palatal shelves are capable of fusion with each other, but fail to fuse with the primary palate in a developmentally delayed manner. Mice carrying an anterior cleft can survive neonatal lethality. Developmental Dynamics 237:1509-1516, 2008. (c) 2008 Wiley-Liss, Inc. |
