Diamide insecticide resistance in transgenic Drosophila and Sf9-cells expressing a full-length diamondback moth ryanodine receptor carrying an I4790M mutation.

Background Resistance to diamide insecticides in Lepidoptera is known to be caused primarily by amino acid changes on the ryanodine receptor (RyR). Recently, two new target site mutations, G4946V and I4790M, have emerged in populations of diamondback moth, Plutella xylostella, as well as in other lepidopteran species, and both mutations have been shown empirically to decrease diamide efficacy. Here, we quantify the impact of the I4790M mutation on diamide activation of the receptor, as compared to alterations at the G4946 locus. Results I4790M when introduced into P. xylostella RyR expressed in an insect derived Sf9 cell line was found to mediate just a 10-fold reduction in chlorantraniliprole efficacy (compared to a 104-fold and 146-fold reduction for G4946E and G4946V variants, respectively), whilst in the field its presence is associated with a ≥ 150-fold reduction. I4790M mediated resistance to flubendiamide was estimated to be >24-fold. When the entire coding sequence of P. xylostella RyR was integrated into Drosophila melanogaster, the I4790M variant conferred ~4.4-fold resistance to chlorantraniliprole and 22-fold resistance to flubendiamide in the 3rd instar larvae, confirming that it imparts only a moderate level of resistance to diamide insecticides. Whereas the I4790M substitution appears to bear no fitness costs in terms of the flies' reproductive capacity, when assessed in a non-competitive environment, it does however have potentially major impacts on mobility at both the larval and adult stage. Conclusions I4790M imparts only a moderate level of resistance to diamide insecticides and potentially confers significant fitness costs to the insect. This article is protected by copyright. All rights reserved.