Effects of canonical Wnt signaling on dorso-ventral specification of the mouse telencephalon

被引:182
作者
Backman, M
Machon, O
Mygland, L
van den Bout, CJ
Zhong, WM
Taketo, MM
Krauss, S
机构
[1] Natl Stem Cell Ctr, N-0349 Oslo, Norway
[2] Univ Oslo, Natl Hosp, Inst Med Microbiol, N-0027 Oslo, Norway
[3] Univ Oslo, Natl Hosp, Ctr Mol Biol & Neurosci, N-0027 Oslo, Norway
[4] Acad Sci Czech Republ, Inst Mol Genet, CR-14220 Prague, Czech Republic
[5] Natl Hosp Norway, Dept Comparat Med, N-0027 Oslo, Norway
[6] Yale Univ, Dept Mol Cellular & Dev Biol, New Haven, CT 06520 USA
[7] Kyoto Univ, Grad Sch Med, Dept Pharmacol, Kyoto 6068501, Japan
关键词
beta-catenin; telencephalon; patterning; progenitor cell identity;
D O I
10.1016/j.ydbio.2004.12.010
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Writ signaling is involved in numerous processes during vertebrate CNS development. In this study, we used conditional Cre/1oxP system in mouse to ablate or activate beta-catenin in the telencephalon in two time windows: before and after the onset of neurogenesis. We show that beta-catenin mediated Wnt signals are required to maintain the molecular identity of the pallium. Inactivation of beta-catenin in the telencephalon before neurogenesis results in downregulated expression of dorsal markers Emx1, Emx2 and Ngn2, and in ectopic up-regulation of ventral markers Gsh2, Mash1 and Dlx2 in the pallium. In contrast, ablation of beta-catenin after the onset of cortical neurogenesis (E11.5) does not result in a dorso-ventral fate shift. In addition, activation of canonical Wnt signaling in the subpallium leads to a repression of ventral telencephalic cell identities as shown by the down-regulation of subpallial markers Dlx2, Nkx2.1, Gsh2, Olig2 and Mash1. This was accompanied with an expansion of dorsal identities ventrally as shown by the expanded expression domains of pallial markers Pax6 and Ngn2. Thus, our data suggest that canonical Wnt signals are involved in maintaining the identity of the pallium by controlling expression of dorsal markers and by suppressing ventral programs from being activated in pallial progenitor cells. (C) 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码:155 / 168
页数:14
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