The short neuropeptide F (sNPF) and NPF receptor (NPFR) genes play important roles in many physiological processes. However, information on the survival-related functions of sNPF and NPFR under different stress conditions is lacking in aphids. In this study, we cloned sNPF and NPFR, and investigated the expression levels of these genes in different developmental stages, wing morphs, and stress conditions of the bird cherryoat aphid (Rhopalosiphum padi L.), an important agricultural pest. The sNPF and NPFR transcript levels varied among developmental stages, and their expression levels in alate females were significantly higher than those in apterous females. In addition, starvation resulted in significantly increased sNPF expression, which then recovered after refeeding. Heat stress and insecticides significantly affected transcription of both genes. sNPF and NPFR knockdown in R. padi using RNA interference revealed optimal interference efficiency at 48 h post-injection. sNPF knockdown significantly decreased adult longevity, 15-d fecundity, and food intake. Additionally, mortality under starvation, insecticides, and heat stress conditions was significantly higher after injection with double-stranded sNPF in R. padi. NPFR knockdown significantly affected food intake and starvation resistance in R. padi. These results strongly indicate that sNPF plays vital roles in food intake, longevity, and reproduction in R. padi, and it can significantly affect the pest's response to stress conditions.
Rhopalosiphum padi is an important global wheat pest. The pyrethroid insecticide bifenthrin is widely used in the control R. padi. We explored the resistance potential, cross-resistance, adaptive costs, and resistance mechanism of R. padi to bifenthrin using a bifenthrin-resistant strain (Rp-BIF) established in laboratory. The Rp-BIF strain developed extremely high resistance against bifenthrin (1033.036-fold). Cross-resistance analyses showed that the Rp-BIF strain had an extremely high level of cross-resistance to deltamethrin (974.483-fold), moderate levels of cross-resistance to chlorfenapyr (34.051-fold), isoprocarb (27.415-fold), imidacloprid (14.819-fold), and thiamethoxam (11.228-fold), whereas negative cross-resistance was observed to chlorpyrifos (0.379-fold). The enzymatic activity results suggested that P450 played an important role in bifenthrin resistance. A super-kdr mutation (M918L) of voltage-gated sodium channel (VGSC) was found in the bifenthrin-resistant individuals. When compared with the susceptible strain (Rp-SS), the Rp-BIF strain was significantly inferior in multiple life table parameters, exhibiting a relative fitness of 0.69. Our toxicological and biochemical studies indicated that multiple mechanisms of resistance might be involved in the resistance trait. Our results provide insight into the bifenthrin resistance of R. padi and can contribute to improve management of bifenthrin-resistant R. padi in the field.
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