| First Author | Wiegering A | Year | 2019 |
| Journal | Dev Biol | Volume | 450 |
| Issue | 2 | Pages | 141-154 |
| PubMed ID | 30953627 | Mgi Jnum | J:276573 |
| Mgi Id | MGI:6315454 | Doi | 10.1016/j.ydbio.2019.02.018 |
| Citation | Wiegering A, et al. (2019) GLI3 repressor but not GLI3 activator is essential for mouse eye patterning and morphogenesis. Dev Biol 450(2):141-154 |
| abstractText | Since 1967, it is known that the loss of GLI3 causes very severe defects in murine eye development. GLI3 is able to act as a transcriptional activator (GLI3-A) or as a transcriptional repressor (GLI3-R). Soon after the discovery of these GLI3 isoforms, the question arose which of the different isoforms is involved in eye formation - GLI3-A, GLI3-R or even both. For several years, this question remained elusive. By analysing the eye morphogenesis of Gli3(XtJ/XtJ) mouse embryos that lack GLI3-A and GLI3-R and of Gli3(Delta699/Delta699) mouse embryos in which only GLI3-A is missing, we revealed that GLI3-A is dispensable in vertebrate eye formation. Remarkably, our study shows that GLI3-R is sufficient for the creation of morphologically normal eyes although the molecular setup deviates substantially from normality. In depth-investigations elucidated that GLI3-R controls numerous key players in eye development and governs lens and retina development at least partially via regulating WNT/beta-CATENIN signalling. |
