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Apoptosis in Xenopus tadpole tail muscles involves Bax-dependent pathways
L M Sachs1, B Abdallah, A Hassan
1Laboratoire de Physiologie Générale et Comparée, Muséum National d'Histoire Naturelle, URA CNRS 90, Paris, France.
Summary
Thyroid hormone (T3) drives apoptosis in Xenopus tadpole tails during metamorphosis. T3 upregulates the Bax gene, a key player in programmed cell death, influencing tail regression.
Area of Science:
- Developmental Biology
- Molecular Biology
- Cellular Biology
Background:
- Apoptosis is crucial for normal development, notably in amphibian metamorphosis.
- Tail regression in tadpoles is a prominent example of apoptosis-driven development.
Purpose of the Study:
- To investigate the role of thyroid hormone (3, 5, 3'-triiodothyronine, T3) in regulating the proapoptotic gene Bax during Xenopus tadpole tail metamorphosis.
- To understand the mechanisms by which T3 influences Bax expression and apoptosis in tail muscle.
Main Methods:
- Analysis of Bax mRNA expression during natural and T3-induced metamorphosis in Xenopus tadpoles.
- Gene transfer of Bax into dorsal tail muscle to assess its role in apoptosis.
- Reporter gene assays using the Bax promoter in dorsal and caudal tail muscles to evaluate transcriptional regulation by T3.
Main Results:
- Bax mRNA expression in tail muscles correlated spatially with apoptosis during metamorphosis.
- T3 treatment induced Bax expression and apoptosis, which was exacerbated by direct Bax gene transfer.
- T3 increased Bax transcription in caudal tail muscle but not in dorsal tail muscle.
Conclusions:
- T3-induced apoptosis in Xenopus tadpole tail muscles involves both Bax-dependent and Bax-independent pathways.
- These apoptotic mechanisms are regulated in a spatially and temporally distinct manner by T3.