Hafeez Abdul, Wang Kou, Liu Wen, Wang Xiao-Ping
Hubei Key Laboratory of Insect Resources Utilization and Sustainable Pest Management, College of Plant Science and Technology, Huazhong Agricultural University, Wuhan, 430070, China.
Hubei Key Laboratory of Insect Resources Utilization and Sustainable Pest Management, College of Plant Science and Technology, Huazhong Agricultural University, Wuhan, 430070, China; Department of Biological Sciences, University of Alberta, Biological Sciences Bldg., Edmonton, Alberta, T6G 2E9, Canada.
Insect Biochem Mol Biol. 2025 Feb;177:104233. doi: 10.1016/j.ibmb.2024.104233. Epub 2024 Nov 30.
Diapause is an adaptive developmental arrest commonly utilized by animals to cope with seasonal changes. Central to this process are hormonal events that bridge photoperiodic cues and physiological changes. In insect reproductive diapause, the absence of juvenile hormone (JH) serves as the primary endocrine event that governs key diapause traits, including ovarian developmental arrest and lipid accumulation. Conventionally, it is believed that the effects of JH are conveyed through the receptor Methoprene-tolerant (Met) and its transcriptional factor Krüppel homolog 1 (Kr-h1). However, our study with the bean bug Riptortus pedestris reveals that JH independently regulates lipid accumulation, bypassing Met and Kr-h1 pathways. R. pedestris enters reproduction under long-day (LD) conditions, while diapause occurs under short-day (SD) conditions. Treatment of SD females with the JH mimic methoprene stimulated reproductive activities, enhancing ovary development and reducing lipid accumulation. In contrast, silencing genes essential for JH biosynthesis in LD females led to pronounced diapause characteristics, including ovarian developmental arrest and substantial lipid accumulation. Interestingly, disruptions in the JH action genes, either Met or Kr-h1, solely affected ovary development, leaving lipid accumulation unchanged, indicating an independent pathway for regulating JH in lipid accumulation. This was further confirmed by RNA interference experiments in SD females, where knockdown of Met or Kr-h1 did not alter the effects of methoprene on lipid reduction. Collectively, these results suggest that JH controls ovary development through the established Met-Kr-h1 pathway, while it modulates lipid accumulation through an alternative, yet to be identified noncanonical pathway during reproductive diapause in R. pedestris.
滞育是动物普遍采用的一种适应性发育停滞，用于应对季节变化。这一过程的核心是连接光周期信号和生理变化的激素事件。在昆虫生殖滞育中，保幼激素（JH）的缺失是控制关键滞育特征的主要内分泌事件，这些特征包括卵巢发育停滞和脂质积累。传统观点认为，JH的作用是通过受体耐甲氧普烯（Met）及其转录因子克氏同源物1（Kr-h1）来传递的。然而，我们对豆蝽Riptortus pedestris的研究表明，JH绕过Met和Kr-h1途径独立调节脂质积累。R. pedestris在长日照（LD）条件下进入繁殖期，而在短日照（SD）条件下发生滞育。用JH类似物甲氧普烯处理SD雌性，刺激了生殖活动，促进了卵巢发育并减少了脂质积累。相反，沉默LD雌性中JH生物合成所必需的基因导致明显的滞育特征，包括卵巢发育停滞和大量脂质积累。有趣的是，JH作用基因Met或Kr-h1的破坏仅影响卵巢发育，脂质积累不变，这表明在脂质积累中存在一条独立的JH调节途径。SD雌性的RNA干扰实验进一步证实了这一点，其中敲低Met或Kr-h1并没有改变甲氧普烯对脂质减少的影响。总的来说，这些结果表明，JH通过已确立的Met-Kr-h1途径控制卵巢发育，而在R. pedestris生殖滞育期间，它通过一条尚未确定的非经典替代途径调节脂质积累。
