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Cited by 337

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Wnt signaling in Xenopus embryos inhibits Bmp4 expression and activates neural development

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Baker, J. C., Beddington, R. S.P., Harland, R. M.·1999·Genes & Development

Abstract

We report a new role for Wnt signaling in the vertebrate embryo: the induction of neural tissue from ectoderm. Early expression of mouse wnt8, Xwnt8, beta-catenin, or dominant-negative GSK3 induces the expression of neural-specific markers and inhibits the expression of Bmp4 in Xenopus ectoderm. We show that Wnt8, but not the BMP antagonist Noggin, can inhibit Bmp4 expression at early gastrula stages. Furthermore, inhibition of beta-catenin activity in the neural ectoderm of whole embryos by a truncated TCF results in a decrease in neural development. Therefore, we suggest that a cleavage-stage Wnt signal normally contributes to an early repression of Bmp4 on the dorsal side of the embryo and sensitizes the ectoderm to respond to neural inducing signals from the organizer. The Wnt targets Xnr3 and siamois have been shown previously to have neuralizing activity when overexpressed. However, antagonists of Wnt signaling, dnXwnt8 and Nxfrz8, inhibit Wnt-mediated Xnr3 and siamois induction, but not neural induction, suggesting an alternative mechanism for Bmp repression and neuralization. Conversely, dnTCF blocks both Wnt-mediated Xnr3 and neural induction, suggesting that both pathways require this transcription factor.

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Metadata

Authors
Baker, J. C., Beddington, R. S. P., & Harland, R. M.
Venue
Genes & Development
Published
1999-12-01
Volume
13
Issue
23
Pages
3149-3159
ISSN
0890-9369 (ISSN-L)
OpenAlex
W2158129482
Cited by
337
References
6
Type
posted content
Language
en
Open access
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CoChat. (2026). Citation check: Wnt signaling in Xenopus embryos inhibits Bmp4 expression and activates neural development. https://app.cochat.ai/papers/10.1101/gad.13.23.3149
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Baker, J. C., Beddington, R. S. P., & Harland, R. M. (1999). Wnt signaling in Xenopus embryos inhibits Bmp4 expression and activates neural development. Genes & Development. https://doi.org/10.1101/gad.13.23.3149

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