高水平表达的P-ERK信号通过调控蛋白酶体活性介导棉铃虫滞育进入的机制研究

Insulin信号通路是调节昆虫滞育的重要信号途径。研究表明insulin信号支路PI3K-AKT-FOXO信号在滞育进入过程中发挥重要作用，然而另一条重要支路Ras-ERK-ETS信号却在滞育进入过程中鲜有研究，其对滞育进入的调控机制尚不清楚。我们研究发现P-ERK在滞育蛹脑中高表达，P-ERK是促进发育的信号，为何会在发育停滞的蛹脑中高表达？其生理意义是什么？进一步实验发现持续高表达P-ERK促进蛋白酶体活性，抑制细胞生长；滞育蛹脑中高水平ROS通过P-InR激活P-ERK。由此，我们首次提出高水平P-ERK调节滞育进入机制：ROS通过P-InR激活P-ERK，进而影响蛋白酶体活性降解发育相关蛋白，抑制发育进程。本项目拟进一步采用western、qPCR、EMSA、启动子活性分析等方法，阐明P-ERK信号调节蛋白酶体活性影响滞育进入的分子机制，为滞育研究以及害虫防治药物开发提供新思路。

Insulin signaling is an important mechanism to regulate insect diapause. Previous study showed that PI3K-AKT-FOXO signal paly a key role in diapause entry, however, the regulation mechanism of another important branch of insulin signaling: Ras-ERK-ETS signal is unclear. Generally, P-ERK signal promote development, however, in the present study, we found that P-ERK was high expression in diapause pupal brains. Further experiments showed that high expression P-ERK promoted proteasome activity and suppressed cell viability; High levels ROS activated P-ERK via P-InR in diapause pupal brains. Therefore we come up with a hypothesis: In the diapause pupal brains, high levels ROS activate P-ERK via avtivating P-InR, then promote proteasome avtivity to degrade development related proteins, and last developmental arrest. In order to provide new ideas to diapause research and pest control drug development, we will further peform western, qPCR, EMSA and promoter activity analysis methods to clarify the mechanism of P-ERK regulate diapause entry via promoting proteasome activity.