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First published online 13 May 2004
doi: 10.1242/dev.01165
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1 Institute of Molecular and Cellular Biosciences, University of Tokyo, 1-1-1
Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan
2 Department of Anatomy, Keio University School of Medicine, Tokyo 160-8582,
Japan
3 Department of Molecular Neurobiology, Institute of DNA Medicine, Jikei
University School of Medicine, 3-25-8 Nishi-shinbashi, Minato-ku, Tokyo
105-8461, Japan
4 National Institute for Physiological Sciences, Myodaiji, Okazaki 444-8585,
Japan
* Author for correspondence (e-mail: ygotoh{at}iam.u-tokyo.ac.jp)
Accepted 27 February 2004
Neural precursor cells (NPCs) have the ability to self-renew and to give rise to neuronal and glial lineages. The fate decision of NPCs between proliferation and differentiation determines the number of differentiated cells and the size of each region of the brain. However, the signals that regulate the timing of neuronal differentiation remain unclear. Here, we show that Wnt signaling inhibits the self-renewal capacity of mouse cortical NPCs, and instructively promotes their neuronal differentiation. Overexpression of Wnt7a or of a stabilized form of ß-catenin in mouse cortical NPC cultures induced neuronal differentiation even in the presence of Fgf2, a self-renewal-promoting factor in this system. Moreover, blockade of Wnt signaling led to inhibition of neuronal differentiation of cortical NPCs in vitro and in the developing mouse neocortex. Furthermore, the ß-catenin/TCF complex appears to directly regulate the promoter of neurogenin 1, a gene implicated in cortical neuronal differentiation. Importantly, stabilized ß-catenin did not induce neuronal differentiation of cortical NPCs at earlier developmental stages, consistent with previous reports indicating self-renewal-promoting functions of Wnts in early NPCs. These findings may reveal broader and stage-specific physiological roles of Wnt signaling during neural development.
Key words: ß-catenin, Wnt, Neurogenesis, Neocortex, Neural precursor cell, Mouse
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