期刊
JOURNAL OF NEUROSCIENCE
卷 26, 期 48, 页码 12620-12630出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3180-06.2006
关键词
neural precursor; beta-catenin; development; cerebral cortex; neurogenesis; cell cycle
资金
- NINDS NIH HHS [F30 NS053303, F30NS053303, R01 NS047191-02, R01 NS047191-01A1, R01 NS047191, R01NS04719, R01 NS047191-03] Funding Source: Medline
Overexpression of beta-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 beta-catenin from cortical neural precursors in vivo causes premature neuronal differentiation. Precursors within the cerebral cortical ventricular zone exhibit robust beta-catenin-mediated transcriptional activation, which is downregulated as cells exit the ventricular zone. Targeted inhibition of beta-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 beta-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 beta-catenin can control the production of cortical neurons and thus regulate cerebral cortical size.
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