GLI3 repressor but not GLI3 activator is essential for mouse eye patterning and morphogenesis
2019
Abstract Since 1967, it is known that the loss of
GLI3causes very severe defects in murine
eye development.
GLI3is able to act as a transcriptional activator (
GLI3-A) or as a transcriptional repressor (
GLI3-R). Soon after the discovery of these
GLI3isoforms, 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
Gli3XtJ/XtJ mouse embryos that lack
GLI3-A and
GLI3-R and of
Gli3Δ699/Δ699 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 developmentand governs lens and retina development at least partially via regulating WNT/β-CATENIN signalling.
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