Wnt signaling controls the timing of oligodendrocyte development in the spinal cord

被引:135
作者
Shimizu, T
Kagawa, T
Wada, T
Muroyama, Y
Takada, S
Ikenaka, K
机构
[1] Kumamoto Univ, Inst Mol Embryol & Genet, Dept Cell Fate Modulat, Kumamoto 8600811, Japan
[2] Natl Inst Basic Biol, Okazaki Natl Res Inst, Natl Inst Physiol Sci, Lab Neurobiol & Bioinformat, Okazaki, Aichi 4448585, Japan
[3] Natl Inst Basic Biol, Okazaki Natl Res Inst, Natl Inst Physiol Sci, Lab Act Transport, Okazaki, Aichi 4448585, Japan
[4] Grad Univ Adv Studies, Sch Life Sci, Dept Physiol Sci, Miura, Kanagawa 2400193, Japan
[5] Kinki Invent Ctr, Japan Sci & Technol Corp JST, Explorat Res Adv Technol ERATO, Kondoh Differentiat Signaling Project,Sakyo Ku, Kyoto 6068305, Japan
[6] Osaka Univ, Inst Mol & Cellular Biol, Suita, Osaka 5650871, Japan
[7] Kyoto Univ, Grad Sch Sci, Ctr Mol & Dev Biol, Sakyo Ku, Kyoto 6068502, Japan
[8] Natl Inst Basic Biol, Ctr Integrat Biosci, Okazaki, Aichi 4448585, Japan
关键词
oligodendrocyte; Wnt; dorsal factor; canonical Wnt/beta-catenin pathway; glial differentiation; sonic hedgehog;
D O I
10.1016/j.ydbio.2005.03.020
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
During spinal cord development, oligodendrocytes are generated from a restricted region of the ventral ventricular zone and then spread out into the entire spinal cord. These events are controlled by graded inductive and repressive signals derived from a local organizing center. Sonic hedgehog was identified as an essential ventral factor for oligodendrocyte lineage specification, whereas the dorsal cue was less clear. In this study, Writ proteins were identified as the dorsal factors that directly inhibit oligodendrocyte development. Writ signaling through a canonical beta-catenin pathway prevents its differentiation from progenitor to an immature state. Addition of rmFz-8/Fc, a Writ antagonist, increased the number of immature oligodendrocytes in the spinal cord explant culture, demonstrating that endogenous Writ signaling controls oligodendrocyte development. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:397 / 410
页数:14
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