Elsevier

Developmental Biology

Volume 239, Issue 1, 1 November 2001, Pages 148-160
Developmental Biology

Regular Article
The Wnt/β-Catenin Pathway Posteriorizes Neural Tissue in Xenopus by an Indirect Mechanism Requiring FGF Signalling

https://doi.org/10.1006/dbio.2001.0431Get rights and content
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Abstract

In order to identify factors involved in posteriorization of the central nervous system, we undertook a functional screen in Xenopus animal cap explants which involved coinjecting noggin RNA together with pools of RNA from a chick somite cDNA library. In the course of this screen, we isolated a clone encoding a truncated form of β-catenin, which induced posterior neural and dorsal mesodermal markers when coinjected with noggin in animal caps. Similar results were obtained with Xwnt-8 and Xwnt-3a, suggesting that these effects are a consequence of activating the canonical Wnt signalling pathway. To investigate whether the activation of posterior neural markers requires mesoderm induction, we performed experiments using a chimeric inducible form of β-catenin. Activation of this protein during blastula stages resulted in the induction of both posterior neural and mesodermal markers, while activation during gastrula stages induced only posterior neural markers. We show that this posteriorizing activity occurs by an indirect and noncell-autonomous mechanism requiring FGF signalling.

Keywords

Xenopus
A/P patterning
Wnt signalling
β-catenin
FGF signalling

Cited by (0)

1

Present address: Laboratory of Vertebrate Embryology, Box 32, Rockefeller University, 1230 York Avenue, New York, NY, 10021.

2

Present address: Section of Gene Function and Regulation, Chester Beatty Laboratories, Institute of Cancer Research, 237 Fulham Road, London SW3 6JB, UK.

3

Present address: Wellcome/CRC Institute of Cancer and Developmental Biology, Tennis Court Road, Cambridge CB2 1QR, UK.

4

Present address: Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, MS 64110.

5

To whom correspondence should be addressed. Fax: 1-816-926-2008. E-mail: [email protected].