Knockdown of farnesyl pyrophosphate synthetase gene TuFPPS by RNAi extends quiescent period and halts molting of the spider mite, Tetranychus urticae.

In insects, farnesyl pyrophosphate synthase (FPPS), a pivotal enzyme in the mevalonate pathway, is crucial in the juvenile hormone (JH)/methyl farnesoate (MF) biosynthesis pathway, particularly regulating the molting process. However, its role in the post-embryonic development and molting in Acari remains unclear. This study therefore investigated the function of TuFPPS in the deutonymphal stage of the two-spotted spider mite, Tetranychus urticae, an important pest in agriculture. Real time quantitative PCR (qPCR) revealed a significant increase in TuFPPS expression in the middle of the quiescent period (28 h). RNA interference (RNAi)-mediated knockdown of TuFPPS caused developmental delays, notably extending the quiescent period and delaying the molting process. Ultimately, the treated mites failed to molt and died with 80% mortality at 108 h before molting, while > 90% of the mites in the control successfully molted. To investigate the potential functions of TuFPPS during the quiescent period and molting process in T. urticae, we performed a genome-wide RNA sequencing following RNAi knockdown of TuFPPS. Four genes were identified based on the thresholds of|FC| ≥ 3 and FDR < 0.05, and these are involved in carbohydrate metabolism, fatty acid and lipid metabolism, amino acid metabolism, and ABC transporters. Altogether, our data suggest that TuFPPS plays a critical role in regulating energy transport, intracellular digestion, and energy supply, as seen in ametabolous insects. These findings lay the foundation for further studies of the molecular mechanism of JH/MF in post-embryonic development and molting in mites, and also identify a potential target for pest control, as demonstrated in T. urticae.