Cell-autonomous β-catenin signaling regulates cortical precursor proliferation

Gregory J. Woodhead, Christopher A. Mutch, Eric C. Olson, Anjen Chenn

Research output: Contribution to journalArticlepeer-review

173 Scopus citations

Abstract

Overexpression of β-catenin, a protein that functions in both cell adhesion and signaling, causes expansion of the cerebral cortical precursor population and cortical surface area enlargement. Here, we find that focal elimination of β-catenin from cortical neural precursors in vivo causes premature neuronal differentiation. Precursors within the cerebral cortical ventricular zone exhibit robust β-catenin-mediated transcriptional activation, which is downregulated as cells exit the ventricular zone. Targeted inhibition of β-catenin signaling during embryonic development causes cortical precursor cells to prematurely exit the cell cycle, differentiate into neurons, and migrate to the cortical plate. These results show that β-catenin-mediated transcriptional activation functions in the decision of cortical ventricular zone precursors to proliferate or differentiate during development, and suggest that the cell-autonomous signaling activity of β-catenin can control the production of cortical neurons and thus regulate cerebral cortical size.

Original languageEnglish (US)
Pages (from-to)12620-12630
Number of pages11
JournalJournal of Neuroscience
Volume26
Issue number48
DOIs
StatePublished - Nov 29 2006
Externally publishedYes

Keywords

  • β-catenin
  • Cell cycle
  • Cerebral cortex
  • Development
  • Neural precursor
  • Neurogenesis

ASJC Scopus subject areas

  • Neuroscience(all)

Fingerprint

Dive into the research topics of 'Cell-autonomous β-catenin signaling regulates cortical precursor proliferation'. Together they form a unique fingerprint.

Cite this