Pest Manag Sci 2020 Dec 01;7612:3954-3964. doi: 10.1002/ps.5944.

Two classic mutations in the linker-helix IIL45 and segment IIS6 of Apolygus lucorum sodium channel confer pyrethroid resistance.

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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 (L1002 F/M906 I) 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. L1002 F, M906 I and L1002 F/M906 I all shifted the voltage dependence of activation in the depolarizing direction. L1002 F, M906 I and L1002 F/M906 I all reduced the amplitude of tail currents induced by type I (bifenthrin and permethrin) and type II (λ-cyhalothrin and deltamethrin). The double mutation, L1002 F/M906 I, reduced integral channel modification by 10-fold compared with the L1002 F and M906 I mutations alone, respectively. Computational analysis based on the model of dual pyrethroid receptors, the two resistance mutations, L1002 F and M906 I 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.

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