| First Author | Pang X | Year | 2021 |
| Journal | Genesis | Volume | 59 |
| Issue | 9 | Pages | e23441 |
| PubMed ID | 34390177 | Mgi Jnum | J:321283 |
| Mgi Id | MGI:6741008 | Doi | 10.1002/dvg.23441 |
| Citation | Pang X, et al. (2021) Sox9CreER-mediated deletion of beta-catenin in palatal mesenchyme results in delayed palatal elevation accompanied with repressed canonical Wnt signaling and reduced actin polymerization. Genesis |
| abstractText | Cleft palate is a good model to pushing us toward a deeper understanding of the molecular mechanisms of spatiotemporal patterns in tissues and organisms because of the multiple-step processes such as elevation and fusion. Previous studies have shown that the epithelial beta-catenin is crucial for palatal fusion, however, the function of the mesenchymal beta-catenin remains elusive. We investigate the role of mesenchymal beta-catenin in palatal development by generating a beta-catenin conditional knockout mouse (CKO) (Sox9CreER; Ctnnb1(F/F) ). We found that the CKO mice exhibited delayed palatal elevation, leading to cleft palate in both in vivo and ex vivo. Abnormal cell proliferation and repressed mesenchymal canonical Wnt signaling were found in the CKO palate. Interestingly, Filamentous actin (F-actin) polymerization was significantly reduced in the palatal mesenchyme of mutant embryos. Furthermore, overexpression of adenovirus-mediated transfection with Acta1 in the mutant could help to elevate the palatal shelves but could not prevent cleft palate in ex vivo. Our results suggest that conditionally knock out beta-catenin in the palatal mesenchyme by Sox9CreER leading to delayed palatal elevation, which results in repressed mesenchymal canonical Wnt signaling, decreased cell proliferation, and reduced actin polymerization, finally causes cleft palate. |
