Abstract

The evolution of resistance to insecticides threatens the sustainable control of many of the world's most damaging insect crop pests and disease vectors. To effectively combat resistance, it is important to understand its underlying genetic architecture, including the type and number of genetic variants affecting resistance and their interactions with each other and the environment. While significant progress has been made in characterizing the individual genes or mutations leading to resistance, our understanding of how genetic variants interact to influence its phenotypic expression remains poor. Here, we uncover a mechanism of insecticide resistance resulting from transposon-mediated insertional mutagenesis of a genetically dominant but insecticide-susceptible allele that enables the adaptive potential of a previously unavailable recessive resistance allele to be unlocked. Specifically, we identify clones of the aphid pest Myzus persicae that carry a resistant allele of the essential voltage-gated sodium channel (VGSC) gene with the recessive M918T and L1014F resistance mutations, in combination with an allele lacking these mutations but carrying a Mutator-like element transposon insertion that disrupts the coding sequence of the VGSC. This results in the down-regulation of the dominant susceptible allele and monoallelic expression of the recessive resistant allele, rendering the clones resistant to the insecticide bifenthrin. These findings are a powerful example of how transposable elements can provide a source of evolutionary potential that can be revealed by environmental and genetic perturbation, with applied implications for the control of highly damaging insect pests.

Highlights

  • The evolution of insecticide resistance represents a serious threat to the sustainable control of insect crop pests and disease vectors [1]

  • Insecticide bioassays were used in combination with molecular genotyping to explore the relationship between kdr/skdr genotype and sensitivity to the pyrethroid bifenthrin in several clones of M. persicae

  • The marked resistance of clones 62H2 and 88H suggests that either kdr/skdr is not inherited as a recessive trait in M. persicae, which is unlikely given the phenotype of 4H, or alternatively that additional genetic mechanisms exist in these clones, which confer resistance to bifenthrin or modify the phenotypic expression of kdr/sdr

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Summary

Introduction

The evolution of insecticide resistance represents a serious threat to the sustainable control of insect crop pests and disease vectors [1]. The intensive and widespread use of insecticides against this species has resulted in the evolution of resistance to many of the compounds used for control [9] This includes the pyrethroid insecticides where resistance has been linked to kdr/skdr mutations in the VGSC. Our findings demonstrate how the adaptive potential of transposable elements can be revealed by environmental and genetic perturbation and that this can have profound and unexpected impacts on resistance They illustrate how combinations of mutations that individually confer no fitness benefit can interact to provide strong context-dependent fitness benefits

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