Glycogen synthase kinase 3β (GSK3β) plays important roles in gene transcription, metabolism, apoptosis, development, and signal transduction. However, its role in the regulation of pupal diapause remains unclear. In this paper, we find that low GSK3β activity in brains of diapause-destined pupae of Helicoverpa armigera is caused by elevated AKT activity. In response to ROS, AKT phosphorylates GSK3β to decrease its activity. In developing pupal brains, GSK3β can activate the transcription factor Smad1, which binds to the promoter region of the ecdysone receptor (EcR) gene and increases its expression. In the presence of 20-hydroxyecdysone (20E), EcR can bind to USP and increase the expression of 20E-response genes, including HR3, for pupal-adult development. In contrast, high levels of ROS in brains of diapause-destined pupae up-regulate p-AKT, which in turn decreases GSK3β activity. Low GSK3β activity causes low expression of EcR/HR3 via down-regulation of Smad1 activity, leading to diapause initiation. These results suggest that low GSK3β activity plays a key role in pupal diapause via ROS/AKT/GSK3β/Smad/EcR/HR3 signaling.

糖原合酶激酶 3β (GSK3β) 在基因转录、代谢、细胞凋亡、发育和信号转导中起重要作用。然而，其在蛹滞育调节中的作用仍不清楚。在本文中，我们发现棉铃虫滞育蛹大脑中的低 GSK3β 活性是由 AKT 活性升高引起的。作为对 ROS 的响应，AKT 磷酸化 GSK3β 以降低其活性。在发育中的蛹脑中，GSK3β 可以激活转录因子 Smad1，后者与蜕皮激素受体 (EcR) 基因的启动子区域结合并增加其表达。在 20-羟基蜕皮激素 (20E) 存在的情况下，EcR 可以与 USP 结合并增加 20E 反应基因（包括 HR3）的表达，用于蛹-成虫发育。相比之下，以滞育为目的的蛹大脑中高水平的 ROS 会上调 p-AKT，从而降低 GSK3β 活性。低 GSK3β 活性通过下调 Smad1 活性导致 EcR/HR3 低表达，从而导致滞育开始。这些结果表明，低 GSK3β 活性通过 ROS/AKT/GSK3β/Smad/EcR/HR3 信号传导在蛹滞育中起关键作用。