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The ecdysone-induced protein 93 is a key factor regulating gonadotrophic cycles in the adult female mosquito Aedes aegypti

Significance In female mosquitoes, repeated blood feedings are essential for maintaining gonadotrophic cycles and serve as the basis for pathogen transmission. We demonstrate that the ecdysone-induced protein 93 (E93), a transcription factor implicated in insect metamorphic transitions, regulates reproductive switches in adult females of the major arboviral vector Aedes aegypti. E93 RNA interference before the first gonadotrophic cycle disrupts the second. E93 silencing disturbed the expression of Hormone Receptor 3 and autophagy, both essential for vitellogenesis termination. Transcriptomic analysis reveals a E93-mediated shutdown of gene expression during the end of a reproductive cycle, particularly genes linked to translation, yolk protein precursors, and metabolism. This study has advanced our understanding of the E93 role in controlling the gonadotrophic cyclicity in female mosquitoes. Repeated blood feedings are required for adult female mosquitoes to maintain their gonadotrophic cycles, enabling them to be important pathogen carriers of human diseases. Elucidating the molecular mechanism underlying developmental switches between these mosquito gonadotrophic cycles will provide valuable insight into mosquito reproduction and could aid in the identification of targets to disrupt these cycles, thereby reducing disease transmission. We report here that the transcription factor ecdysone-induced protein 93 (E93), previously implicated in insect metamorphic transitions, plays a key role in determining the gonadotrophic cyclicity in adult females of the major arboviral vector Aedes aegypti. Expression of the E93 gene in mosquitoes is down-regulated by juvenile hormone (JH) and up-regulated by 20-hydroxyecdysone (20E). We find that E93 controls Hormone Receptor 3 (HR3), the transcription factor linked to the termination of reproductive cycles. Moreover, knockdown of E93 expression via RNAi impaired fat body autophagy, suggesting that E93 governs autophagy-induced termination of vitellogenesis. E93 RNAi silencing prior to the first gonadotrophic cycle affected normal progression of the second cycle. Finally, transcriptomic analysis showed a considerable E93-dependent decline in the expression of genes involved in translation and metabolism at the end of a reproductive cycle. In conclusion, our data demonstrate that E93 acts as a crucial factor in regulating reproductive cycle switches in adult female mosquitoes.