昆虫变态发育过程中的细胞自噬和凋亡

Autophagy and apoptosis in insect cells during metamorphosis

在昆虫变态期,幼虫组织发生退化或消亡,原因在于蜕皮甾醇激素(ecdysteroid),即通常所说的蜕皮激素,诱导这些组织的细胞发生了自噬(autophagy)和凋亡(apoptosis)的程序性细胞死亡(programmed cell death,PCD)。一般情况下,自噬途径构成一种饥饿应激适应性以避免细胞的死亡,表现为低水平Cvt泡(Cvt vesicle)和自噬体(autophagosome)对部分胞质溶胶、蛋白聚集体和细胞器的吞噬和降解。昆虫进入变态发育时,由于蜕皮激素的激活,由遗传级联系统调控的PCD机制被启动,低水平的常态自噬转入高水平的自噬并同时诱发凋亡,细胞进入不可逆的死亡,导致幼虫组织在变态期退化或消亡。对果蝇Drosophila变态期PCD机制中最重要的发现是:(1)在自噬发生的PI3KⅠ-Tor和PI3KⅢ的分子通路中,由自噬相关蛋白Atg1引发的高水平自噬能够诱导凋亡;(2)蜕皮激素诱导表达的βFTZ-F1,E93,BR-C,E74A等转录因子不但激活凋亡的Caspases通路,还能诱导自噬的发生。

During insect metamorphosis, degeneration or dissolution of larval tissues was involved in programmed cell death （PCD） including autophagy and apoptosis induced by ecdysteroids. Autophagy, which usually responds to hungry to avoid cell death, appears as a low-level Cvt vesicle and autophagosome to swallow and dissolve partial cytosol, protein aggregates and cellular organelles. PCD pathway is initiated by ecdysteroids and regulated by genetic cascade system during the period metamorphosis. The initiation of PCD pathway by ecdysteroids turns the low-level normal auto of insect phagy to high-level one and triggers apoptosis at the same time, and leads to irreversible death. Subsequently larval tissues degenerate or dissolve completely. The most important discoveries of PCD in fruit fly Drosophila metamorphosis include ： （ 1 ） In the molecular pathways of PI3KI-Tor and PI3KIII, high-level autophagy initiated by Atgl （autophagy-related protein 1 ） can induce apoptosis; （2） Transcription factors induced by eedysteroids, including βFTZ-F1, E93, BR-C and E74A, can not only activate the apoptosis pathway, but also induce autophagy pathway.