通过卵巢滤泡上皮细胞的间隙（patency）吸收卵黄蛋白原是昆虫卵黄发生的关键环节。大多数昆虫中，保幼激素（JH）-钙信号通路在Na+/K+-ATPase依赖的卵巢patency调控中起到关键的作用，然而分子机制不明确。基于此，本项目拟以飞蝗JH - patency开展工作，旨在分析JH钙信号通路激活Na+/K+-ATPase的分子机制。利用RNA干扰（RNAi）筛选出通路中激活Na+/K+-ATPase的钙信号转导因子--- PKC，CaMKII。通过质谱数据鉴定通路中PKC、CaMKII以及Na+/K+-ATPase翻译后修饰位点，分析这些信号转导分子的活化机制。而后运用定点突变、蛋白亚细胞定位、RNAi、免疫共沉淀等技术，最终阐明PKC、CaMKII激活Na+/K+-ATPase的分子机制。本项目研究中的关键信号通路的阐明，为利用生殖分子机制作为害虫绿色防控提供理论支撑。

The uptake of vitellogenin by the oocyte via intercellular spaces (patency) between the ovarian follicular epithelial cells is an necessary stage during the insect oogenesis. In various insects, Juvenile hormone (JH)-calcium signaling pathway regulates ovarian patency which is dependent on the action of Na+/K+-ATPase, whereas the related mechanism is unclear. In regard of that, we will focus on the analysis of the molecular mechanism involved in the JH-triggered Na+/K+-ATPase activity through calcium signaling pathways in Locusta moratoria. RNA interference (RNAi) will be used to screened calcium signal transduction factors (i.e. Protein Kinase C, PKC and Ca2+/calmodulin-dependent protein kinase II, CaMKII) involved in the activation of Na+/K+-ATPase through calcium signal pathways during JH-induced ovarian patency. Posttranslational modification will be analyzed by mass spectrometric analysis for the activation mechanism of PKC, CaMKII and Na+/K+-ATPase involved in the JH-triggered ovarian patency in L. moratoria. Subsequently, the molecular mechanism of Na+/K+-ATPase activated by PKC and CaMKII will be identified by site-directed mutagenesis, RNAi and Co-Immunoprecipitation (Co-IP). Finally, the molecular mechanism of Na+/K+-ATPase activated by JH-calcium signaling pathways will be clarified. The key signaling pathways researched in this study will supply the theoretic support for pest control by reproductive mechanism.