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The Journal of Neuroscience, November 29, 2006, 26(48):12620-12630; doi:10.1523/JNEUROSCI.3180-06.2006

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 Previous Article

Development/Plasticity/Repair
Cell-Autonomous -Catenin Signaling Regulates Cortical Precursor Proliferation

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

Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611

Correspondence should be addressed to Anjen Chenn, Department of Pathology, Northwestern University, 303 East Chicago Avenue, Ward Building 6-204, Chicago, IL 60611. Email: achenn{at}northwestern.edu

Overexpression of -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 -catenin from cortical neural precursors in vivo causes premature neuronal differentiation. Precursors within the cerebral cortical ventricular zone exhibit robust -catenin-mediated transcriptional activation, which is downregulated as cells exit the ventricular zone. Targeted inhibition of -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 -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 -catenin can control the production of cortical neurons and thus regulate cerebral cortical size.

Key words: neural precursor; -catenin; development; cerebral cortex; neurogenesis; cell cycle

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Received July 25, 2006; revised Oct. 18, 2006; accepted Oct. 19, 2006.

Correspondence should be addressed to Anjen Chenn, Department of Pathology, Northwestern University, 303 East Chicago Avenue, Ward Building 6-204, Chicago, IL 60611. Email: achenn{at}northwestern.edu

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