BMP antagonists and FGF signaling contribute to different domains of the neural plate in Xenopus

被引:28
|
作者
Wills, Andrea E. [1 ,2 ]
Choi, Vivian M. [3 ]
Bennett, Margaux J. [1 ,2 ]
Khokha, Mustafa K. [4 ]
Harland, Richard M. [1 ,2 ]
机构
[1] Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA
[2] Univ Calif Berkeley, Ctr Integrat Genom, Berkeley, CA 94720 USA
[3] Univ Chicago, Med Scientist Training Program, Chicago, IL 60637 USA
[4] Yale Univ, Sch Med, Dept Pediat & Genet, New Haven, CT 06520 USA
关键词
Xenopus; Sox2; Neural induction; BMP antagonist; beta-catenin; SU5402; FIBROBLAST-GROWTH-FACTOR; SPEMANN ORGANIZER; BETA-CATENIN; FOREBRAIN DEVELOPMENT; DORSAL DEVELOPMENT; GENE-EXPRESSION; FACTORS CHORDIN; NERVOUS-SYSTEM; INDUCTION; INHIBITION;
D O I
10.1016/j.ydbio.2009.11.008
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
In ectodermal explants from Xenopus embryos, inhibition of BMP signaling is sufficient for neural induction, leading to the idea that neural fate is the default state in the ectoderm. Many of these experiments assayed the action of BMP antagonists on animal caps, which are relatively naive explants of prospective ectoderm, and different results have led to debate regarding both the mechanism of neural induction and the appropriateness of animal caps as an assay system. Here we address whether BMP antagonists are only able to induce neural fates in pre-patterned explants, and the extent to which neural induction requires FGF signaling. We suggest that some discrepancies in conclusion depend on the interpretations of sox gene expression, which we show not only marks definitive neural tissue, but also tissue that is not yet committed to neural fates. Part of the early sox2 domain requires FGF signaling, but in the absence of organizer signaling, this domain reverts to epidermal fates. We also reinforce the evidence that ectodermal explants are naive, and that explants that lack any dorsal prepattern are readily neuralized by BMP antagonists, even when FGF signaling is inhibited. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:335 / 350
页数:16
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