| First Author | Chen D | Year | 2020 |
| Journal | Dev Biol | Volume | 458 |
| Issue | 1 | Pages | 88-97 |
| PubMed ID | 31669335 | Mgi Jnum | J:284162 |
| Mgi Id | MGI:6390126 | Doi | 10.1016/j.ydbio.2019.10.022 |
| Citation | Chen D, et al. (2020) FRS2alpha-dependent cell fate transition during endocardial cushion morphogenesis. Dev Biol 458(1):88-97 |
| abstractText | Atrioventricular valve development requires endothelial-to-mesenchymal transition (EndMT) that induces cushion endocardial cells to give rise to mesenchymal cells crucial to valve formation. In the adult endothelium, deletion of the docking protein FRS2alpha induces EndMT by activating TGFbeta signaling in a miRNA let-7-dependent manner. To study the role of endothelial FRS2alpha during embryonic development, we generated mice with an inducible endothelial-specific deletion of Frs2alpha (FRS2alpha(iECKO)). Analysis of the FRS2alpha(iECKO) embryos uncovered a combination of impaired EndMT in AV cushions and defective maturation of AV valves leading to development of thickened, abnormal valves when Frs2alpha was deleted early (E7.5) in development. At the same time, no AV valve developmental abnormalities were observed after late (E10.5) deletion. These observations identify FRS2alpha as a pivotal controller of cell fate transition during both EndMT and post-EndMT valvulogenesis. |
