Li Shan, Wang Xueli, Lu Haoran, Raikhel Alexander S, Zou Zhen
State Key Laboratory of Animal Biodiversity Conservation and Integrated Pest Management, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
University of Chinese Academy of Sciences, Beijing, China.
Commun Biol. 2025 Jul 2;8(1):983. doi: 10.1038/s42003-025-08428-7.
The regulation of mosquito reproduction at the transcriptional level is well understood, but the translational mechanisms remain unclear. Here, we find that lysyl-tRNA synthetase (KARS) is essential for translational regulation and governs mosquito fecundity in a hormone-dependent manner. RNA interference silencing of KARS severely inhibits ovarian maturation and impairs mosquito fecundity. Polysome profiling shows enhanced translation initiation in KARS-deficient mosquitoes, as supported by increased phosphorylation of p70 ribosomal protein S6 kinase and decreased phosphorylation of the translation initiation factor eIF2α. By contrast, incorporated puromycin reveals a reduction in the synthesis of nascent polypeptides such as vitellogenin. Further analysis of ribosome profiling sequencing indicates that the dysregulation of mRNA translation in KARS-deficient mosquitoes was caused by ribosome stalling. Furthermore, the knockdown of KARS results in a significant increase in JH and a decline in 20E, thereby forcing the mosquitoes to maintain prereproductive status and preventing the 20E-activated vitellogenesis. This study demonstrates the function of KARS in regulating reproduction during the gonadotrophic cycle, hence providing insights into the potential control of disease-transmitting mosquitoes.
在转录水平上对蚊子繁殖的调控已得到充分了解，但翻译机制仍不清楚。在此，我们发现赖氨酰 - tRNA合成酶（KARS）对于翻译调控至关重要，并以激素依赖的方式控制蚊子的繁殖力。KARS的RNA干扰沉默严重抑制卵巢成熟并损害蚊子的繁殖力。多核糖体分析显示，在缺乏KARS的蚊子中翻译起始增强，这得到了p70核糖体蛋白S6激酶磷酸化增加和翻译起始因子eIF2α磷酸化减少的支持。相比之下，掺入的嘌呤霉素显示新生多肽如卵黄原蛋白的合成减少。核糖体分析测序的进一步分析表明，缺乏KARS的蚊子中mRNA翻译失调是由核糖体停滞引起的。此外，KARS的敲低导致保幼激素显著增加和20E减少，从而迫使蚊子维持生殖前状态并阻止20E激活的卵黄发生。本研究证明了KARS在调节促性腺周期中的繁殖功能，从而为潜在控制传播疾病的蚊子提供了见解。
