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Updated: Aug 10, 2026

Stem cell-like Xenopus Embryonic Explants to Study Early Neural Developmental Features In Vitro and In Vivo
Published on: February 2, 2016
Distinctive gene profiles occur at key points during natural metamorphosis in the Xenopus laevis tadpole tail
Nik Veldhoen1, Doug Crump, Kate Werry
1Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia, Canada.
Abstract:
Thyroid hormones (THs) are essential for tadpole metamorphosis into a juvenile frog; however, a complex interplay between additional hormones and signaling events also contributes to this dramatic developmental phase. A major mechanism of TH action is the nuclear receptor-mediated regulation of gene transcription of responsive genes. By using the precocious metamorphic model, several genes have been identified as TH responsive in the regressing tail. Many of these genes also exhibit altered expression during natural metamorphosis. Although identification of these genes provides insight into the mechanism whereby TH acts, complex interplay between TH and other hormones and the developmental stage-dependency of tissue responses contribute to the timing and coordination of metamorphic events. We investigated the temporal gene expression profile in Xenopus laevis tadpole tails from premetamorphosis through metamorphic climax by using a combination of a novel frog cDNA array containing 420 genes and quantitative real-time PCR. Seventy-nine genes were identified whose steady-state mRNA expression levels were altered in the tadpole tail during natural metamorphosis, of which 34 have previously been identified to be TH responsive in frogs or mammals. Of these genes, 75 clustered into 13 groups that displayed distinct developmental expression profiles. The levels of 28 transcripts were altered during premetamorphosis, 31 during prometamorphosis, and 43 with the onset of tail regression. This work establishes an important baseline for determining the mechanisms whereby tissues undergo differing metamorphic fates.
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