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Updated: Jul 6, 2026

Spinal Cord Transection In Xenopus laevis Tadpoles
Published on: December 10, 2021
Requirement for Wnt and FGF signaling in Xenopus tadpole tail regeneration
1Centre for Regenerative Medicine, Department of Biology and Biochemistry, University of Bath, Bath BA2 7AY, UK.
Abstract:
We have investigated the requirement for the FGF and Wnt/beta-catenin pathways for Xenopus tadpole tail regeneration. Pathways were modified either by treatment with small molecules or by induction of transgene expression with heat shocks. Regeneration is inhibited by treatment with the FGF inhibitor SU5402, or by activation of a dominant negative FGF receptor, or by activation of expression of the Wnt inhibitor Dkk1. Agents promoting Wnt activity: the small molecule BIO, or a constitutively active form of beta-catenin, led to an increased growth rate. Combination of a Wnt activator with FGF inhibitor suppressed regeneration, while combination of a Wnt inhibitor with a FGF activator allowed regeneration. This suggests that the Wnt activity lies upstream of the FGF activity. Expression of both Wnt and FGF components was inhibited by activation of noggin, suggesting that BMP signalling lies upstream of both Wnt and FGF. The results show that the molecular mechanism of Xenopus tadpole tail regeneration is surprisingly similar to that of the Xenopus limb bud and the zebrafish caudal fin, despite the difference of anatomy.
Insights
Fibroblast Growth Factor (FGF) and Wnt/beta-catenin pathways are crucial for Xenopus tadpole tail regeneration. BMP signaling acts upstream of both Wnt and FGF pathways, influencing regeneration.
Area of Science:
- Developmental Biology
- Regenerative Medicine
- Molecular Biology
Background:
- Tail regeneration in Xenopus tadpoles is a complex process involving intricate molecular signaling pathways.
- Understanding the specific roles of Fibroblast Growth Factor (FGF) and Wnt/beta-catenin signaling is key to deciphering regenerative mechanisms.
Purpose of the Study:
- To investigate the necessity of FGF and Wnt/beta-catenin pathways in Xenopus tadpole tail regeneration.
- To elucidate the hierarchical relationship between BMP, Wnt, and FGF signaling in tail regeneration.
Main Methods:
- Utilized small molecule inhibitors (e.g., SU5402, BIO) to modulate pathway activity.
- Employed heat shock to induce transgene expression, including dominant-negative FGF receptor and Wnt inhibitor Dkk1.
- Analyzed the effects of pathway manipulation on tail regeneration and growth rates.
Main Results:
- FGF and Wnt pathway inhibition (SU5402, Dkk1) suppressed tail regeneration.
- Wnt pathway activation (BIO, constitutively active beta-catenin) enhanced regeneration rate.
- BMP signaling (via noggin) was found to be upstream of both Wnt and FGF pathways.
Conclusions:
- Wnt pathway activity appears to lie upstream of FGF pathway activity in tail regeneration.
- The molecular mechanisms governing Xenopus tadpole tail regeneration share similarities with limb bud and caudal fin regeneration.
- BMP signaling is a critical upstream regulator of both Wnt and FGF pathways in this regenerative model.
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