Abstract
The diamondback moth, Plutella xylostella, is a damaging pest of cruciferous crops, and has evolved resistance to many of the insecticides used for control, including members of the diamide class. Previous work on the molecular basis of resistance to diamides has documented mutations in the target-site, the ryanodine receptor, in resistant populations of P. xylostella worldwide. In contrast the role of metabolic resistance to this insecticide class is significantly less clear. Here we show that overexpression of a flavin-dependent monooxgenase (FMO) confers resistance to the diamide chlorantraniliprole in P. xylostella. Transcriptome profiling of diamide resistant strains, with and without target-site resistance, revealed constitutive over-expression of several transcripts encoding detoxification enzymes compared to susceptible strains. Two of these, CYP6BG1, and PxFMO2 were particularly highly overexpressed (33,000 and 14,700-fold, respectively) in a resistant strain (HAW) lacking target-site resistance. After 17 generations without diamide selection the resistance of the HAW strain fell by 52-fold and the expression of PxFMO2 by > 1300-fold, however, the expression of CYP6BG1 declined by only 3-fold. Generation of transgenic Drosophila melanogaster expressing these genes demonstrated that PxFMO2, but not CYP6BG1, confers resistance in vivo. Overexpression of PxFMO2 in the HAW strain is associated with mutations, including a putative transposable element insertion, in the promoter of this gene. These enhance the expression of a reporter gene when expressed in a lepidopteran cell line suggesting they are, at least in part, responsible for the overexpression of PxFMO2 in the resistant strain. Our results provide new evidence that insect FMOs can be recruited to provide resistance to synthetic insecticides.
Highlights
The diamondback moth, Plutella xylostella, is one of the most destructive insect pests of cruciferous crops worldwide resulting in estimated costs to the global economy of US$4–5 billion per annum (Zalucki et al, 2012)
The primary mechanism of resistance to diamide insecticides in P. xylostella populations described to date has been target-site based, and the role, if any, of alternative mechanisms in resistance to this class of insecticides has remained unclear (Troczka et al, 2017)
Our data demonstrate that metabolic mechanisms can confer resistance to the diamide chlorantranilprole in P. xylostella and highlight a novel enzyme family that has not been previously implicated in resistance to this insecticide class
Summary
The diamondback moth, Plutella xylostella, is one of the most destructive insect pests of cruciferous crops worldwide resulting in estimated costs to the global economy of US$4–5 billion per annum (Zalucki et al, 2012). In attempts to minimise crop damage caused by this pest growers have relied heavily on the use of synthetic insecticides for control Their intensive use, in Asia, has resulted in the emergence of potent resistance to a range of different insecticide classes (Furlong et al, 2013). The diamide insecticides, comprising flubendiamide, chlorantraniliprole and cyantraniliprole, are a relatively new class of insecticide that were introduced to control P. xylostella from 2007 (Nauen, 2006; Troczka et al, 2017). They initially proved extremely effective at controlling this pest, in part, because they were not compromised by resistance mechanisms that had evolved to older compounds.
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