Department of Entomology, China Agricultural University, Beijing, China.
Pest Manag Sci. 2020 Sep;76(9):3038-3045. doi: 10.1002/ps.5854. Epub 2020 Apr 29.
Neonicotinoid insecticide imidacloprid acts on insect nicotinic acetylcholine receptors (nAChRs). The mechanisms of insect resistance to imidacloprid include target-site alteration and increased detoxification metabolism. In Bradysia odoriphaga, cytochrome P450 monooxygenase has been found involved in metabolic resistance to imidacloprid. However, the situation of target-site related resistance to imidacloprid in B. odoriphaga is still unknown.
Nine field-collected B. odoriphaga populations showed various sensitivities to imidacloprid compared with the susceptible (SS) strain, including susceptibility, decreased susceptibility, low resistance, moderate resistance and high resistance. Seven nAChR subunit genes including α1, α2, α3, α7, α8, β1 and β3, were examined for site mutation and changes in transcription levels in field populations. No nAChR polymorphism potentially related to the resistant phenotypes was found. However, differential expression of nAChR subunit genes was found in imidacloprid resistant field population. In high imidacloprid resistant population LC-2 (93.14-fold resistance), the transcription levels of α1, α2 and β1 subunits were significantly down-regulated, while the transcription levels of α3 and α8 subunits were significantly up-regulated, compared with that in SS strain. In addition, imidacloprid acute exposure induced differential expression of nAChR subunit genes in B. odoriphaga. Furthermore, RNA interference (RNAi) suppressed the transcriptional expression of Boα1 and Boβ1, and decreased mortality of B. odoriphaga by 23.03% and 18.69%, respectively, when treated with imidacloprid.
These results indicated that, although no target-site mutation was found in imidacloprid resistant B. odoriphaga population, the reduced expression of α1 and β1 subunits contributed to B. odoriphaga resistance to imidacloprid. © 2020 Society of Chemical Industry.
新烟碱类杀虫剂吡虫啉作用于昆虫烟碱型乙酰胆碱受体（nAChRs）。昆虫对吡虫啉产生抗药性的机制包括靶标改变和解毒代谢增加。在小菜蛾中，已发现细胞色素 P450 单加氧酶参与了对吡虫啉的代谢抗性。然而，小菜蛾对吡虫啉的靶标相关抗性情况仍不清楚。
与敏感（SS）菌株相比，9 个田间采集的小菜蛾种群对吡虫啉表现出不同的敏感性，包括敏感性、降低敏感性、低抗药性、中抗药性和高抗药性。检测了包括α1、α2、α3、α7、α8、β1和β3 在内的 7 个 nAChR 亚基基因的靶标突变和转录水平变化。未发现与抗性表型相关的潜在 nAChR 多态性。然而，在抗吡虫啉的田间种群 LC-2 中发现 nAChR 亚基基因的差异表达。在高抗吡虫啉的 LC-2 种群（93.14 倍抗性）中，α1、α2 和β1 亚基的转录水平显著下调，而α3 和α8 亚基的转录水平显著上调，与 SS 株系相比。此外，吡虫啉急性暴露诱导小菜蛾 nAChR 亚基基因的差异表达。此外，RNA 干扰（RNAi）抑制 Boα1 和 Boβ1 的转录表达，当用吡虫啉处理时，小菜蛾的死亡率分别降低了 23.03%和 18.69%。
这些结果表明，尽管在抗吡虫啉的小菜蛾种群中未发现靶标突变，但α1 和β1 亚基的表达降低导致了小菜蛾对吡虫啉的抗性。© 2020 化学工业协会。
