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<p>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 <i>KARS</i> severely inhibits ovarian maturation and impairs mosquito fecundity. Polysome profiling shows enhanced translation initiation in <i>KARS</i>-deficient mosquitoes, as supported by increased phosphorylation of p70 ribosomal protein S6 kinase and decreased phosphorylation of the translation initiation factor eIF2<i>α</i>. 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 <i>KARS</i>-deficient mosquitoes was caused by ribosome stalling. Furthermore, the knockdown of <i>KARS</i> 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.</p>

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Lysyl-tRNA synthetase orchestrates translation and hormone signaling during reproduction in Aedes aegypti mosquitoes

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月2日

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  • Shan Li,
  • Xueli Wang,
  • Haoran Lu,
  • Alexander S. Raikhel,
  • Zhen Zou

摘要

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.