PyR2 中丙氨酸到甘氨酸的取代赋予钠通道对 I 型拟除虫菊酯的抗性。

Alanine to glycine substitution in the PyR2 confers sodium channel resistance to Type I pyrethroids.

作者信息

Chen Mengli, Wang Likui, Zhou Xiangyi, Chen Guoxing, Xu Zhanyi, Yan Ru, Qian Jiali, Zhu Guonian, Wu Shaoying, Wu Huiming

机构信息

The Key Laboratory for Quality Improvement of Agricultural Products of Zhejiang Province, College of Advanced Agricultural Sciences, Zhejiang A&F University, Hangzhou, China.

Sanya Nanfan Research Institute, Hainan University, Sanya, China.

出版信息

Pest Manag Sci. 2025 Apr;81(4):2248-2256. doi: 10.1002/ps.8625. Epub 2024 Dec 30.

DOI:10.1002/ps.8625

PMID:39740097

Abstract

BACKGROUND

Aedes aegypti is a primary urban vector of dengue, yellow fever, Zika and chikungunya worldwide. Pyrethroid insecticides are the most effective insecticides for controlling Ae. aegypti. However, pyrethroid resistance has developed due to the long-term overuse of the insecticides, and many knockdown resistance (kdr) mutations have been identified in the resistant populations. A1007G, an alanine to glycine substitution, was found in resistant Ae. aegypti from Vietnam and Malaysia, which has always co-existed with F1534C and V1016G. However, the role of A1007G in pyrethroid resistance and the linkage of A1007G and F1534C or V1016G remain unknown.

RESULTS

In this study, we examined the effects of mutations on the sodium channel gating properties and pyrethroid sensitivity in Xenopus oocytes. We found mutations A1007G, A1007G + F1534C and A1007G + V1016G + F1534C shifted the voltage dependence of activation in the depolarizing direction. Mutations A1007G + F1534C and A1007G + V1016G + F1534C shifted the voltage dependence of inactivation in the depolarizing direction. Both mutations A1007G and F1534C reduced the channel sensitivity to two Type I pyrethroids, permethrin and bifenthrin, and synergistic effects were observed between mutations A1007G and F1534C. However, none of the mutations, A1007G, F1534C and A1007G + F1534C affected the channel sensitivity to two Type II pyrethroids, deltamethrin and cypermethrin. Furthermore, triple mutations A1007G + V1016G + F1534C significantly reduced the channel sensitivity to both Type I and Type II pyrethroids.

CONCLUSION

We identified A1007G had a distinct effect on sodium channel sensitivity to Type I, but not to Type II pyrethroids, also A1007G exhibited synergistic effects with F1534C to Type I pyrethroids, which will provide a fundamental insight into the distinct molecular interactions between insect sodium channel and Type I or Type II pyrethroids. © 2024 Society of Chemical Industry.

摘要

背景

埃及伊蚊是全球登革热、黄热病、寨卡病毒病和基孔肯雅热的主要城市传播媒介。拟除虫菊酯类杀虫剂是控制埃及伊蚊最有效的杀虫剂。然而，由于长期过度使用这些杀虫剂，已产生了拟除虫菊酯抗性，并且在抗性种群中已鉴定出许多击倒抗性（kdr）突变。在来自越南和马来西亚的抗性埃及伊蚊中发现了A1007G（丙氨酸替换为甘氨酸），它一直与F1534C和V1016G共存。然而，A1007G在拟除虫菊酯抗性中的作用以及A1007G与F1534C或V1016G的连锁关系仍然未知。

结果

在本研究中，我们研究了这些突变对非洲爪蟾卵母细胞钠通道门控特性和拟除虫菊酯敏感性的影响。我们发现突变A1007G、A1007G + F1534C和A1007G + V1016G + F1534C使激活的电压依赖性向去极化方向偏移。突变A1007G + F1534C和A1007G + V1016G + F1534C使失活的电压依赖性向去极化方向偏移。A1007G和F1534C这两个突变均降低了通道对两种I型拟除虫菊酯（氯菊酯和联苯菊酯）的敏感性，并且在A1007G和F1534C突变之间观察到协同效应。然而，A1007G、F1534C以及A1007G + F1534C这些突变均未影响通道对两种II型拟除虫菊酯（溴氰菊酯和氯氰菊酯）的敏感性。此外，三重突变A1007G + V1016G + F1534C显著降低了通道对I型和II型拟除虫菊酯的敏感性。