钙信号途径在昆虫变态发育中的功能及激素调控

全变态昆虫的幼虫组织在变态发育过程中发生程序性细胞死亡，而蜕皮激素(20E)则可以促进昆虫变态及程序性细胞死亡。我们在前期研究中发现20E可以促进细胞内质网中的内钙离子释放和细胞外钙离子内流，推测钙离子信号途径参与了20E诱导的变态及程序性细胞死亡，但目前尚缺乏足够的实验证据说明钙离子信号在昆虫变态和程序性细胞死亡中的功能，对参与钙信号途径的主要蛋白、作用机理、激素调控也不清楚。因此本课题拟以棉铃虫为材料，研究钙信号途径在昆虫变态发育中的功能及激素调控, 包括鉴定参与20E调控细胞内钙离子增加的主要蛋白; 研究钙信号途径主要蛋白在昆虫变态发育及程序性细胞死亡中的功能; 分析激素对细胞内钙离子水平的调控及机理;研究钙信号途径的上游调控分子及下游效应分子，阐明蜕皮激素调控细胞内钙离子增加的分子机制及在昆虫变态发育及程序性细胞死亡中的作用，充实昆虫变态的分子机理,为害虫控制提供新的靶标基因。

The larval tissues perform programmed cell death (PCD) during metamorphosis in holometabolic insects. The steroid hormone 20-hydroxyecdysone (20E) promotes PCD and metamorphosis. We observed that 20E triggers calcium (Ca2+) increase in the cells, including intracellular calcium release from endoplasmic reticulum and extracellular calcium influx, suggesting the involvement of the calcium signaling in the 20E-induced metamorphosis and PCD. However, the evidences are short to demonstrate the function of calcium in insect metamorphosis and PCD. The involved proteins, mechanisms and hormonal regulation in the calcium signaling are unclear. Therefore, we are going to investigate the function and hormonal regulation of the calcium signaling pathway in insect metamorphosis and PCD using Helicoverpa armigera as a model. The scientific questions include: identification of the major proteins involved in 20E-induced calcium increase, the function of the calcium pathway proteins in the PCD and metamorphosis, the hormonal regulation of 20E on the calcium levels and mechanism, and the upstream factors participating in 20E-induced calcium increase. This study may demonstrate the mechanism of 20E-induced calcium increase and its role in PCD and metamorphosis, and produce new conception and enrich our knowledge in insect metamorphosis. The functional genes identified in calcium signaling may become the targets in insect control.