Cell-Autonomous β-Catenin Signaling Regulates Cortical Precursor Proliferation

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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.