Mutations of two acidic residues at the cytoplasmic end of segment IIIS6 of an insect sodium channel have distinct effects on pyrethroid resistance.

Journal Article (Journal Article)

Mutations in sodium channels are known to confer knockdown resistance to pyrethroid insecticides, such as permethrin and cypermethrin, in various agricultural pests and disease vectors. Double mutations, D3i28 V and E3i32 G, were detected in cypermethrin-resistant Helicoverpa armigera and Heliothis virescens populations. However, the role of the two mutations in pyrethroid resistance remains unclear. In this study, we introduced the mutations into the cockroach sodium channel, BgNav 1-1a, and examined their effects on channel gating and pyrethroid sensitivity in Xenopus oocytes. D3i28 V alone and the double mutation, D3i28 V/E3i32 G, shifted the voltage dependence of activation in the depolarizing direction by 15 mV and 20 mV, respectively, whereas E3i32 G had no significant effect. D3i28 V reduced the amplitude of tail currents induced by permethrin and NRDC 157 (Type I pyrethroids) and deltamethrin and cypermethrin (Type II pyrethroids), whereas E3i32 G alone had no effect. Intriguingly, the amplitude of Type II pyrethroid-induced tail current from D3i28 V/E3i32 G channels was similar to that of BgNav 1-1a channels, but the decay of the tail currents was accelerated. Such effects were not observed for Type I pyrethroid-induced tail currents. Computational analysis based on the model of dual pyrethroid receptors on insect sodium channels predicted D3i28 V and E3i32 G exert their effects on channel gating and pyrethroid action via allosteric mechanisms. Our results not only illustrate the distinct effect of the D3i28 V/E3i32 G double mutations on Type I vs. Type II pyrethroids, but also reinforce the concept that accelerated decay of tail currents can be an effective mechanism of pyrethroid resistance to Type II pyrethroids.

Full Text

Duke Authors

Cited Authors

  • Chen, M; Du, Y; Nomura, Y; Zhu, G; Zhorov, BS; Dong, K

Published Date

  • March 2017

Published In

Volume / Issue

  • 82 /

Start / End Page

  • 1 - 10

PubMed ID

  • 28111191

Pubmed Central ID

  • PMC5730327

Electronic International Standard Serial Number (EISSN)

  • 1879-0240

International Standard Serial Number (ISSN)

  • 0965-1748

Digital Object Identifier (DOI)

  • 10.1016/j.ibmb.2017.01.007

Language

  • eng