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Mitotic WNT signalling orchestrates neurogenesis in the developing neocortex.

Fabio Da Silva1, Kaiqing Zhang1, Anneline Pinson2

  • 1Division of Molecular Embryology, DKFZ, Heidelberg, Germany.

The EMBO Journal
|August 25, 2021
PubMed
Summary

WNT/STOP signaling is crucial for mouse neocortex development. This pathway stabilizes key proteins, promoting neurogenesis by regulating neural progenitor cell division and fate during mitosis.

Keywords:
LRP6WNT signallingmicrocephalymitosisneurogenesis

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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Cell Biology

Background:

  • The role of WNT/β-catenin signaling in neocortex development is debated, with conflicting evidence on its effects on progenitor self-renewal versus differentiation.
  • WNT/STOP signaling stabilizes proteins during the G2/M phase by inhibiting glycogen synthase kinase (GSK3)-mediated degradation.

Purpose of the Study:

  • To investigate the role of WNT/STOP signaling in mouse neocortex development.
  • To elucidate the mechanisms by which WNT/STOP signaling influences neural progenitor cell behavior and neurogenesis.

Main Methods:

  • Analysis of mice deficient for cyclin Y and cyclin Y-like 1 (Ccny/l1), key regulators of WNT/STOP signaling.
  • Examination of neural progenitor cell proliferation, cell cycle progression, and division patterns.
  • Identification of WNT/STOP signaling targets using molecular and genetic approaches.

Main Results:

  • Ccny/l1-deficient mice exhibit significantly reduced neurogenesis in the developing neocortex.
  • Basal progenitors show delayed cell cycle progression and a drastic decrease in numbers.
  • Apical progenitors display reduced asymmetric division linked to increased apical-basal astral microtubules.
  • Sox4 and Sox11, neurogenic transcription factors, are identified as direct GSK3 targets stabilized by WNT/STOP signaling in basal progenitors during mitosis.

Conclusions:

  • WNT/STOP signaling plays a critical role in driving cortical neurogenesis.
  • Mitosis is identified as a key regulatory phase for determining neural progenitor cell fate within the WNT/STOP pathway.