A Drosophila model to study the functions of TWIST orthologs in apoptosis and proliferation
A Drosophila model to study the functions of TWIST orthologs in apoptosis and proliferation
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DOI：
10.1038/sj.cdd.4401222
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发表时间：
2003-06-01
影响因子：
12.4
通讯作者：
Silber, J
中科院分区：
文献类型：
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作者：
Gullaud, M;Delanoue, R;Silber, J
扭转基因的特点是它在几个物种的肌肉发生中的作用。此外，在哺乳动物培养的细胞中，已经表明twist是一种潜在的癌基因拮抗p53依赖性细胞凋亡。为了在体内研究twist在细胞凋亡和增殖中的作用，我们构建了允许异位表达不同twist直系同源物的转基因果蝇系。我们报告：（i）果蝇扭曲诱导细胞凋亡和激活收割机启动子，（ii）线虫扭曲诱导逮捕的增殖没有细胞凋亡，和（iii）人类扭曲保留其在哺乳动物培养细胞中观察到的潜力，拮抗果蝇p53依赖性细胞凋亡。此外，我们表明，人类扭曲是能够诱导果蝇细胞增殖。数据表明，人类twist拮抗果蝇p53的途径可能是保守的。因此，这些转基因系构成了一个强大的工具，以确定目标和人类扭曲的修改器。
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.