神经肽Tachykinin调控棉铃虫中肠脂肪代谢分子机理

昆虫中肠脂肪代谢被认为是TK/TKR/PKA信号通路参与调控的。TK一旦与G-蛋白受体结合，就以环腺苷酸（cAMP）作为第二信使进行信号转导，cAMP通过激活蛋白激酶Ａ（Protein kinase A，PKA）进而通过磷酸化作用激活下游靶标蛋白，从而调控下游一系列生理生化活动。目前，TK信号转导中的关键途径---cAMP/PKA信号途径介导的脂肪代谢分子机制，尤其是其激活/抑制下游信号分子的鉴定及功能研究仍是未知。本项目拟以棉铃虫为模式昆虫，采用磷酸化蛋白质组学、 RNAi、GC/MS等生理生化与分子生物学技术，对TK/TKR/PKA信号通路在中肠脂肪代谢中的分子特性、PKA调控的下游靶标蛋白的鉴定及其在脂肪代谢过程中的功能等开展研究。该项目为进一步研究HaTK调控棉铃虫中肠脂肪代谢分子机制、发现潜在的抗虫靶标基因提供新的思路。

The neuropeptide tachykinin(TK) producted in endocrine cell of insect midgut regulate lipid homeostasis. Once binding with its G-protein receptor, TK uses cAMP as second messenger. cAMP activates its down-stream signal, TK/TKR/PKA pathway, which regulates a serial of unknown targeted signals and thus influence lipid homeostasis. However the molecular characteristic of PKA, PKA effect lipid homeostasis, PKA-mediated down-stream signal molecules still keep elusive. In this proposed study, the associated studies regarding to cAMP/PKA action，especially PKA-regulated targeted molecules and their corresponding functions in midgut are studied by phosphoproteomics, RNAi, GC/MS etc. This study, using Helicoverpa armigera as a model, will not only elucidate the molecular mechanism of lipid metabolism in insect, but also provide a new approach for special targets for chemical control.