| First Author | San Miguel S | Year | 2011 |
| Journal | Dev Dyn | Volume | 240 |
| Issue | 2 | Pages | 357-64 |
| PubMed ID | 21246652 | Mgi Jnum | J:167836 |
| Mgi Id | MGI:4880799 | Doi | 10.1002/dvdy.22546 |
| Citation | San Miguel S, et al. (2011) Ephrin reverse signaling controls palate fusion via a PI3 kinase-dependent mechanism. Dev Dyn 240(2):357-64 |
| abstractText | Secondary palate fusion requires adhesion and epithelial-to-mesenchymal transition (EMT) of the epithelial layers on opposing palatal shelves. This EMT requires transforming growth factor beta3 (TGFbeta3), and its failure results in cleft palate. Ephrins, and their receptors, the Ephs, are responsible for migration, adhesion, and midline closure events throughout development. Ephrins can also act as signal-transducing receptors in these processes, with the Ephs serving as ligands (termed 'reverse' signaling). We found that activation of ephrin reverse signaling in chicken palates induced fusion in the absence of TGFbeta3, and that PI3K inhibition abrogated this effect. Further, blockage of reverse signaling inhibited TGFbeta3-induced fusion in the chicken and natural fusion in the mouse. Thus, ephrin reverse signaling is necessary and sufficient to induce palate fusion independent of TGFbeta3. These data describe both a novel role for ephrins in palate morphogenesis, and a previously unknown mechanism of ephrin signaling. Developmental Dynamics 240:357-364, 2011. (c) 2011 Wiley-Liss, Inc. |
