BACKGROUND
Pyrethroids are classified as type I and type II for distinct symptomology. Voltage‐gated sodium channel is a primary target of pyrethroids. Mutations of the insect sodium channel have been identified to result in resistance to pyrethroids. Double mutation (L1002F/M906I) was detected in field‐strain of Apolygus lucorum (Meyer‐Dür). Although, it was illuminated the function of the same position mutation in other pests, it is necessary to demonstrate the role in A. lucorum .
RESULTS
In this study, we examined the effects of mutations on channel gating and pyrethroid sensitivity in Xenopus oocytes. L1002F, M906I and L1002F/M906I all shifted the voltage dependence of activation in the depolarizing direction. L1002F, M906I and L1002F/M906I all reduced the amplitude of tail currents induced by type I (bifenthrin and permethrin) and type II (λ‐cyhalothrin and deltamethrin). The double mutation, L1002F/M906I, reduced integral channel modification by 10‐fold compared with the L1002F and M906I mutations alone, respectively. Computational analysis based on the model of dual pyrethroid receptors, the two resistance mutations, L1002F and M906I are facing two opposite sides of this newly identified pocket. Both mutations affect the optimal binding of the ligands by changing the shape of the pocket but in different ways.
CONCLUSION
Our results illustrate the distinct effect of mutations on pyrethroids. It is predicted with computer modeling that these mutations allosterically affect pyrethroid binding. © 2020 Society of Chemical Industry