Impact of mutations in the voltage-gated sodium channel on insecticide resistance in the soybean aphid Aphis glycines (Hemiptera: Aphididae)

Management of the soybean aphid, Aphis glycines, relies on foliar-application of insecticides, most commonly pyrethroids like lambda-cyhalothrin. Failure of lambda-cyhalothrin to control soybean aphid outbreaks has been reported in the Upper Midwest, and resistance has been confirmed in laboratory assays. Insecticide resistance is associated with non-synonymous mutations in pyrethroid target sites of the voltage-gated sodium channel subunit h1 (vgsc-h1) gene, comprising four known genotypes that vary in degree of resistance to lambda-cyhalothrin. Our objective was to evaluate the contribution of each vgsc-h1 mutation to aphid resistant phenotypes. This was accomplished by applying double-stranded RNA (dsRNA) probes that target specific vgsc-h1 mutations, causing transient RNA interference (RNAi)-based silencing through sequence-specific mRNA degradation. We created a set of dsRNA probes matching vgsc-h1 resistance alleles found in Iowa and Minnesota field populations, and one probe that combines all these vgsc-h1 mutations. The probes were applied to aphids that correspond to the specific genotype by topical application in laboratory assays both with and without lambda-cyhalothrin. The combined probe was applied to all four distinct vgsc-h1 aphid genotypes. On average, combining dsRNA with the insecticide increased mortality by 72% compared to the insecticide alone across all colonies, indicating that these mutations are major contributors to pyrethroid resistant phenotypes in field populations. Our results established genotype to phenotype associations and determined that the dsRNA probe with all four mutations mediated silencing across the four colony genotypes.