Juvenile hormone counteracts the bHLH-PAS transcription factors MET and GCE to prevent caspase-dependent programmed cell death in Drosophila
Juvenile hormone counteracts the bHLH-PAS transcription factors MET and GCE to prevent caspase-dependent programmed cell death in Drosophila
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DOI：
10.1242/dev.033712
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发表时间：
2009-06-15
期刊：
影响因子：
4.6
通讯作者：
Li, Sheng
中科院分区：
文献类型：
--
作者：
Liu, Ying;Sheng, Zhentao;Li, Sheng
保幼激素（JH）调节昆虫的许多发育和生理事件，但其分子机制尚不清楚。在这里，我们报告说，基因消融的果蝇环腺（JH源）的咽侧体细胞导致JH缺乏症，蛹致死性和早熟和增强程序性细胞死亡（PCD）的幼虫脂肪体。在JH缺陷动物的脂肪体中，Dronc和Drice，这两个半胱天冬酶基因对蜕皮激素20-羟基蜕皮激素（20 E）诱导的PCD至关重要，被显著上调。这些结果表明，JH拮抗20 E诱导的PCD通过限制Dronc和Drice的mRNA水平。通过20 E处理和20 E受体EcR的RNA干扰，在JH缺陷动物中进一步证实了JH对20 E诱导的脂肪体PCD的拮抗作用。此外，MET和GCE，参与JH作用的bHLH-PAS转录因子，显示通过上调Dronc和Drice诱导PCD。在Met和gce缺陷动物中，Dronc和Drice下调，而在Met过表达脂肪体中，Dronc和Drice显著上调，导致早熟和增强的PCD，并且这种上调可以通过应用JH激动剂甲氧普烯来抑制。我们首次证明，JH抵消MET和GCE，以防止caspase依赖的PCD控制脂肪体重塑和幼虫蛹变态果蝇。
Juvenile hormone (JH) regulates many developmental and physiological events in insects, but its molecular mechanism remains conjectural. Here we report that genetic ablation of the corpus allatum cells of the Drosophila ring gland ( the JH source) resulted in JH deficiency, pupal lethality and precocious and enhanced programmed cell death (PCD) of the larval fat body. In the fat body of the JH-deficient animals, Dronc and Drice, two caspase genes that are crucial for PCD induced by the molting hormone 20-hydroxyecdysone (20E), were significantly upregulated. These results demonstrated that JH antagonizes 20E-induced PCD by restricting the mRNA levels of Dronc and Drice. The antagonizing effect of JH on 20E-induced PCD in the fat body was further confirmed in the JH-deficient animals by 20E treatment and RNA interference of the 20E receptor EcR. Moreover, MET and GCE, the bHLH-PAS transcription factors involved in JH action, were shown to induce PCD by upregulating Dronc and Drice. In the Met- and gce-deficient animals, Dronc and Drice were downregulated, whereas in the Met- overexpression fat body, Dronc and Drice were significantly upregulated leading to precocious and enhanced PCD, and this upregulation could be suppressed by application of the JH agonist methoprene. For the first time, we demonstrate that JH counteracts MET and GCE to prevent caspase-dependent PCD in controlling fat body remodeling and larval-pupal metamorphosis in Drosophila.