A steroid-triggered transcriptional hierarchy controls salivary gland cell death during Drosophila metamorphosis
A steroid-triggered transcriptional hierarchy controls salivary gland cell death during Drosophila metamorphosis
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DOI：
10.1016/s1097-2765(00)80439-6
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发表时间：
2000-03-01
期刊：
影响因子：
16
通讯作者：
Thummel, CS
中科院分区：
文献类型：
--
作者：
Jiang, CA;Lamblin, AFJ;Thummel, CS
类固醇激素蜕皮激素信号的阶段特异性程序性细胞死亡的幼虫唾液腺在果蝇变态。这种反应之前是蜕皮激素触发的基因表达开关，其中diap 2死亡抑制剂被抑制，收割者（rpr）和头部退化缺陷（hid）死亡激活剂被诱导。在这里，我们表明rpr是由蜕皮激素受体复合物通过rpr启动子中的基本反应元件直接诱导的。广泛复合物（BR-C）是rpr和hid转录所必需的，而E74 A是最大水平的hid诱导所必需的。diap 2诱导依赖于β FTZ-F1，而E75 A和E75 B各自足以抑制diap 2。这项研究确定了果蝇程序性细胞死亡的转录调节因子，并提供了类固醇信号和程序性细胞死亡反应之间的直接联系。
The steroid hormone ecdysone signals the stage-specific programmed cell death of the larval salivary glands during Drosophila metamorphosis. This response is preceded by an ecdysone-triggered switch in gene expression in which the diap2 death inhibitor is repressed and the reaper (rpr) and head involution defective (hid) death activators are induced. Here we show that rpr is induced directly by the ecdysonereceptor complex through an essential response element in the rpr promoter. The Broad-Complex (BR-C) is required for both rpr and hid transcription, while E74A is required for maximal levels of hid induction. diap2 induction is dependent on beta FTZ-F1, while E75A and E75B are each sufficient to repress diap2. This study identifies transcriptional regulators of programmed cell death in Drosophila and provides a direct link between a steroid signal and a programmed cell death response.