Abstract
The twist gene has been characterized for its role in myogenesis in several species. In addition, in mammalian cultured cells, it has been shown that twist is a potential oncogene antagonizing p53-dependent apoptosis. To study, in vivo, the role of twist in apoptosis and proliferation, we constructed transgenic Drosophila lines allowing ectopic expression of different twist orthologs. We report that: (i) Drosophila twist induces apoptosis and activates the reaper promoter, (ii) nematode twist induces arrest of proliferation without apoptosis, and (iii) human twist retains its potentialities observed in mammalian cultured cells and antagonizes Drosophila p53-dependent apoptosis. In addition, we show that human twist is able to induce cell proliferation in Drosophila. Data suggest that the pathway by which human twist antagonizes Drosophila p53 could be conserved. These transgenic lines thus constitute a powerful tool to identify targets and modifiers of human twist.
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Abbreviations
- bHLH:
-
basic helix–loop–helix
- MTWIST:
-
mouse TWIST
- IGF-1:
-
insulin-like growth factor 1
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Acknowledgements
The authors are very grateful to M Baylies, A Fire, J Abrams, F Perrin-Schmidtt for fly stocks and cDNA. They thank J Abrams for helpful comments. They acknowledge the excellent technical assistance of A Dutriaux, B Legois, and MC Gendron. The work was supported by the ARC and ATC vieillissement.
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Gullaud, M., Delanoue, R. & Silber, J. A Drosophila model to study the functions of TWIST orthologs in apoptosis and proliferation. Cell Death Differ 10, 641–651 (2003). https://doi.org/10.1038/sj.cdd.4401222
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DOI: https://doi.org/10.1038/sj.cdd.4401222


