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Published on: January 26, 2013
Developmental cell death during Xenopus metamorphosis involves BID cleavage and caspase 2 and 8 activation
D Du Pasquier1, V Rincheval, L Sinzelle
1Laboratoire de Transgenèse et Génétique des Amphibiens, CNRS UMR 8080, IBAIC, Université Paris-Sud, Orsay Cedex, France.
Summary
During Xenopus metamorphosis, the BID protein and Caspases-2 and -8 initiate apoptosis, leading to tadpole organ regression. This study reveals a key step in the programmed cell death pathway during amphibian development.
Area of Science:
- Developmental Biology
- Cell Death Research
- Molecular Biology
Background:
- Tadpole organ loss during metamorphosis primarily occurs via apoptosis.
- The mitochondrial death pathway, involving Bax, caspase-3, and caspase-9, is implicated.
- Upstream regulators of Bax activation in this process remain largely unknown.
Purpose of the Study:
- To investigate the role of BH3-only proteins, specifically BID, in the upstream regulation of apoptosis during Xenopus metamorphosis.
- To elucidate the involvement of caspases-2 and -8 in tail regression.
- To understand the hormonal regulation and organ autonomy of this apoptotic pathway.
Main Methods:
- Quantitative analysis of Xenopus bid transcript levels during metamorphosis.
- Monitoring of Caspase-2 and -8 mRNA levels and activity.
- Utilizing BIDGFP transgenic Xenopus tadpoles to observe tail regression dynamics.
- Employing caspase-8 inhibitors to assess their impact on BIDGFP cleavage and metamorphosis.
Main Results:
- Xenopus bid transcript levels and Caspase-2 and -8 mRNA levels/activity increase during metamorphosis in regressing larval cells.
- Accelerated tail regression observed in BIDGFP transgenic tadpoles.
- Caspase-8 inhibitors blocked BIDGFP cleavage during natural and T(3)-induced metamorphosis.
Conclusions:
- The thyroid hormone (T(3)) induces an organ-autonomous apoptotic pathway during Xenopus metamorphosis.
- This pathway involves the cell death executioners BID, Caspase-2, and Caspase-8.
- BID acts upstream in initiating the caspase cascade leading to tadpole organ regression.
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