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GLI3 repressor but not GLI3 activator is essential for mouse eye patterning and morphogenesis.

Antonia Wiegering1, Patrick Petzsch2, Karl Köhrer2

  • 1Institute for Animal Developmental and Molecular Biology, Heinrich Heine University, 40225 Düsseldorf, Germany.

Developmental Biology
|April 7, 2019
PubMed
Summary

GLI3 transcriptional repressor (GLI3-R) is sufficient for normal eye development, while GLI3 activator (GLI3-A) is not essential. GLI3-R regulates key eye development genes and WNT/β-CATENIN signaling.

Keywords:
DKKEye developmentHedgehogLensRetinaWNTβ-CATENIN

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Area of Science:

  • Developmental Biology
  • Genetics
  • Molecular Biology

Background:

  • The role of GLI3 isoforms in vertebrate eye development has been a long-standing question since 1967.
  • GLI3 functions as both a transcriptional activator (GLI3-A) and repressor (GLI3-R).

Purpose of the Study:

  • To determine whether GLI3-A, GLI3-R, or both are essential for eye morphogenesis.
  • To elucidate the specific roles of GLI3 isoforms in eye development.

Main Methods:

  • Analysis of eye development in Gli3XtJ/XtJ mouse embryos (lacking both GLI3-A and GLI3-R).
  • Analysis of eye development in Gli3Δ699/Δ699 mouse embryos (lacking only GLI3-A).

Main Results:

  • GLI3-A is dispensable for vertebrate eye formation.
  • GLI3-R alone is sufficient for morphologically normal eye development, despite molecular differences.
  • GLI3-R regulates key eye development genes, including those involved in lens and retina formation, partly through WNT/β-CATENIN signaling.

Conclusions:

  • GLI3-R plays a crucial role in eye development, controlling essential molecular pathways.
  • The GLI3 activator function is not required for normal eye morphogenesis.