蜕皮激素和IIS-TORC1信号的分子互作

Interplay between 20-hydroxyecdysone and insulin/TORC1 signals

蜕皮激素信号主导调控昆虫的蜕皮和变态,决定昆虫的发育时间;IIS-TORC1信号整合生长因子、激素、营养和能量信号,决定昆虫的生长速率。蜕皮激素和IIS-TORC1信号之间发生3种分子互作:(1)IIS-TORC1信号促进前胸腺和卵巢合成蜕皮激素前体。(2)在蜕皮和变态期间,蜕皮激素抑制脂肪体细胞内IIS-TORC1信号、Myc的转录、细胞生长及其内分泌功能,导致脑神经分泌细胞分泌胰岛素样肽的功能减弱,从而降低昆虫全身性的IIS-TORC1信号。(3)在幼虫摄食期间,胰岛素信号抑制FOXO的转录活性,降低了蜕皮激素受体EcR的转录共激活因子DOR编码基因的转录水平,从而阻碍了蜕皮激素信号传导。蜕皮激素信号和IIS-TORC1信号协同调控发育时间和生长速率共同决定昆虫的个体大小。

Ecdysone induces molting and metamorphosis, as well as regulating the timing of development in insects, whereas the IIS-TORC1 signaling pathway integrates growth factors, nutrition and energy to control growth rate. Interplay between these two pathways occurs in three ways： （1） IIS-TORC1 signaling activates ecdysone synthesis in the prothoracic gland; （2） ecdysone inhibits both IIS-TORC1 signaling and transcription of Myc in fat bodies. In other words, ecdysone inhibits systemic IIS-TORC1 signaling by inhibiting tissue growth and the endocrine function of fat bodies; （3） activated insulin signaling inhibits ecdysone signaling by inhibiting transcription of DOR, which is regulated by the transcriptional activity of FOXO. Thus,the interplay between ecdysone signaling and IIS-TORC1 signaling allows the coordination of growth rate and developmental timing, thereby determining final body size.