昆虫滞育是备受关注的基础性生物学问题。已发现一些化学物质可以改变滞育的表达，它们可为滞育机理的阐明提供线索，也为滞育操控提供了工具。KK-42既可影响柞蚕等的蛹滞育（项目组的研究结果），又可影响家蚕等的胚胎滞育，是已知的唯一既可影响不同物种滞育又可影响不同滞育类型的化合物。KK-42延迟柞蚕等蛹滞育的解除，推测是KK-42抑制了前胸腺的蜕皮激素合成途径，或者抑制了Torso介导的PTTH-MAPK途径，从而影响了滞育解除的进程。项目以KK-42的靶器官——前胸腺为研究对象，对提出的假设进行检验，将追踪KK-42处理后滞育蛹中前胸腺的形态和发育变化；比较KK-42处理后体内KK-42与蜕皮激素动态变化过程；检测KK-42对蜕皮激素合成途径相关基因表达的影响；调查KK-42对Torso途径相关基因表达的影响。结果可为理解KK-42延迟作蚕等昆虫蛹滞育解除的调控机理提供分子生理学方面的证据。

Insect diapause is one of critical issues of concern in Biology. Several chemical agents have been known to be capable of manipulating the expression of insect diapause, thus not only provide insights into mechanisms regulating diapause but also potentially offer tools for diapause manipulation. Among agents known to alter diapause responses is KK-42 (1-benzyl-5-[(E)-2,6-dimethyl-1,5-heptadienyl] imidazole), an imidazole derivative that functions as an insect growth regulator. Earlier studies demonstrated that this chemical can affect embryonic diapause, and our recent studies reveal that it also influences pupal diapause. Thus, KK-42 is rather unique in being capable of influencing diapause in both different species as well as different diapausing stages of development. The effect of KK-42 on impairment of pupal dipause termination we presented is likely the result of KK-42 modulating ecdysteroidogenesis in pupal prothotacic glands (PGs) by inhibiting ecdysteroid synthesis pathway, or restraining Torso pathway that mediates PTTH-triggered MARK pathway, thereby shunting more into diapause. .To address this hypothesis, in this project, we will chose diapausing pupae of A. pernyi as the model insect, which is not only a classic organism for studying diapause regulation but also an economically important insect used for silk production and as a human food source in China. This project aims to explore the modulatory mechanism of KK-42 on impairment of pupal dipause termination by investigating morphological and developmental changes in the PGs that is the target organ of KK-42, dynamic changing process between KK-42 and ecdysteroids of the titer, effect of KK-42 on the mRNA expression of genes related to ecdysteroid synthesis pathway (Nvd, Spo, Phm, Dib, Sad, and Shd), and effect of KK-42 on the expression of genes related to Torso pathway that mediates PTTH-triggered MARK pathway (Torso, Ras, Raf, MEK, and ERK). Our project will provide insights into understanding the modulatory mechanism of KK-42 on impairment of pupal dipause termination in insects.