A steroid-triggered transcriptional hierarchy controls salivary gland cell death during Drosophila metamorphosis
被引:223
作者:
Jiang, CA
论文数: 0引用数: 0
h-index: 0
机构:Univ Utah, Dept Human Genet, Howard Hughes Med Inst, Salt Lake City, UT 84112 USA
Jiang, CA
Lamblin, AFJ
论文数: 0引用数: 0
h-index: 0
机构:Univ Utah, Dept Human Genet, Howard Hughes Med Inst, Salt Lake City, UT 84112 USA
Lamblin, AFJ
Steller, H
论文数: 0引用数: 0
h-index: 0
机构:Univ Utah, Dept Human Genet, Howard Hughes Med Inst, Salt Lake City, UT 84112 USA
Steller, H
Thummel, CS
论文数: 0引用数: 0
h-index: 0
机构:
Univ Utah, Dept Human Genet, Howard Hughes Med Inst, Salt Lake City, UT 84112 USAUniv Utah, Dept Human Genet, Howard Hughes Med Inst, Salt Lake City, UT 84112 USA
Thummel, CS
[1
]
机构:
[1] Univ Utah, Dept Human Genet, Howard Hughes Med Inst, Salt Lake City, UT 84112 USA
[2] MIT, Dept Biol, Howard Hughes Med Inst, Cambridge, MA 02139 USA
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.