RNA interference-mediated silencing of ecdysone receptor (EcR) gene causes lethal and sublethal effects on melon aphid, Aphis gossypii

Ecdysone receptor (EcR) plays important roles in molting, metamorphosis, and reproduction of insects. EcR ortholog and its function in melon aphid Aphis gossypii have not been documented yet. RNA interference (RNAi) is a reverse-genetic approach used to study functional genomics, but recently, it has also shown promise as a novel tool that could be used to control insect pests. In this study, reverse transcription-PCR (RT-PCR), quantitative real-time PCR (qPCR), RNAi, and bioassays were employed to isolate EcR gene and investigate its knock-down effects on aphids. The lethal and sublethal effects were also studied after silencing the EcR gene. The results showed that EcR gene is highly expressed (P < 0.006) in 2(nd) nymphal stage of A. gossypii while expression was statistically lower in all other developmental stages. Knock-down of EcR gene caused up to 43 and 68% mortality in 2(nd) instar nymphs after feeding dsEcR for 48 and 72 h, respectively, compared to the control. Moreover, RNAi-induced silencing of EcR gene caused sublethal effects on surviving aphids. Significantly lower longevity (about 42%) and fecundity (about 44.22%) were observed in insects fed with dsEcR solution at their nymphal stage. Analysis of gene expression showed that the mortality rates and the lowered longevity and fecundity were attributable to the down-regulation of EcR gene by RNA interference technology. Taken together, our results demonstrate that EcR is an essential gene for aphid growth and development and could be a potential target gene for the development of an RNAi-based bio-aphicide.

Automated summary

The Ecdysone receptor (EcR) is an essential gene for aphid growth and development. This study demonstrates the potential of using RNA interference (RNAi) technology to control aphids by silencing the EcR gene. The results suggest that EcR could be a target gene for the development of RNAi-based bio-aphicide.