Virginia Polytechnic Institute and State University, Department of Entomology, Molecular Physiology and Toxicology Laboratory Blacksburg, VA 24061, USA.
Virginia Polytechnic Institute and State University, Department of Entomology, Molecular Physiology and Toxicology Laboratory Blacksburg, VA 24061, USA; School of Neuroscience, Fralin Life Science Institute, Virginia Tech Center for Drug Discovery, Center for Emerging Zoonotic and Arthropod-borne Diseases, Virginia Tech, Blacksburg, VA 24061, USA.
Pestic Biochem Physiol. 2024 Aug;203:105972. doi: 10.1016/j.pestbp.2024.105972. Epub 2024 Jun 3.
The Drosophila melanogaster MD-RR strain contains an Rdl mutation (A301S) resulting in resistance to several insecticide classes viz. phenyl pyrazoles (e.g., fipronil), cyclodienes (e.g., dieldrin), and chlorinated aliphatic hydrocarbons (e.g., lindane). Fitness costs are commonly observed with resistant insect populations as side effects of the genetic change conferring the resistant phenotype. Because of fitness costs, reversion from the resistant to susceptible genotype and phenotype is common. However, the Rdl genotype in D. melanogaster appears to allow the flies to maintain the resistant genotype/phenotype without selective pressure and with minimal fitness costs. We provide evidence that compensation for the Rdl mutation influences the cholinergic system, where an increase in acetylcholinesterase gene expression and enzyme activity results in neurophysiological changes and cross resistance to a carbamate insecticide (propoxur oral resistance ratio (RR) of 63) and an organophosphate insecticide (dichlorvos oral RR of 7). Such cross resistance was not previously reported with the initial collection and testing of this strain. In addition to acetylcholinesterase, the Rdl mutation influences the expression of the muscarinic acetylcholine receptor subtype-B, resulting in resistance to non-selective muscarinic compounds (pilocarpine and atropine). Collectively, these results indicate that the Rdl mutation (A301S) at GABA-gated ionophore complex influences the physiology of the cholinergic system, leading to resistance to established insecticide classes. Additionally, this mutation may impact the effectiveness of insecticides targeting novel sites, like muscarinic receptors.
黑腹果蝇 MD-RR 品系含有一个 Rdl 突变（A301S），导致对几类杀虫剂产生抗性，例如苯基吡唑类（如氟虫腈）、环二烯类（如狄氏剂）和氯化脂肪族烃类（如林丹）。抗性昆虫种群中通常会观察到适应度代价，这是赋予抗性表型的遗传变化的副作用。由于适应度代价，抗性基因型向敏感基因型和表型的回复很常见。然而，黑腹果蝇中的 Rdl 基因型似乎允许果蝇在没有选择压力的情况下维持抗性基因型/表型，并且适应度代价最小。我们提供的证据表明，Rdl 突变的补偿会影响胆碱能系统，其中乙酰胆碱酯酶基因表达和酶活性的增加会导致神经生理变化和对氨基甲酸酯杀虫剂（丙氧脲口服抗性比 (RR) 为 63）和有机磷杀虫剂（敌敌畏口服 RR 为 7）的交叉抗性。这种交叉抗性在最初收集和测试该品系时并未被报道过。除了乙酰胆碱酯酶外，Rdl 突变还影响毒蕈碱型乙酰胆碱受体亚型-B 的表达，导致对非选择性毒蕈碱化合物（毛果芸香碱和阿托品）的抗性。总的来说，这些结果表明，GABA 门控离子通道复合物中的 Rdl 突变（A301S）会影响胆碱能系统的生理学，导致对已建立的杀虫剂类别产生抗性。此外，这种突变可能会影响针对新型靶标（如毒蕈碱受体）的杀虫剂的效果。
