Low expression levels of nicotinic acetylcholine receptor subunits Boα1 and Boβ1 are associated with imidacloprid resistance in Bradysia odoriphaga

摘要: Background Neonicotinoid insecticide imidacloprid acts on insect nicotinic acetylcholine receptors (nAChRs). The mechanisms of resistance to include target-site alteration and increased detoxification metabolism. In Bradysia odoriphaga, cytochrome P450 monooxygenase has been found involved in metabolic imidacloprid. However, the situation related B. odoriphaga is still unknown. Results Nine field-collected populations showed various sensitivities compared with susceptible (SS) strain, including susceptibility, decreased low resistance, moderate high resistance. Seven nAChR subunit genes α1, α2, α3, α7, α8, β1 β3, were examined for site mutation changes transcription levels field populations. No polymorphism potentially resistant phenotypes was found. differential expression population. population LC-2 (93.14-fold resistance), α2 subunits significantly down-regulated, while α3 α8 up-regulated, that SS strain. addition, acute exposure induced odoriphaga. Furthermore, RNA interference (RNAi) suppressed transcriptional Boα1 Boβ1, mortality by 23.03% 18.69%, respectively, when treated Conclusion These results indicated that, although no population, reduced α1 contributed © 2020 Society Chemical Industry.