V101I and R81T mutations in the nicotinic acetylcholine receptor β1 subunit are associated with neonicotinoid resistance in Myzus persicae.

Abstract

The peach-potato aphid, Myzus persicae (Sulzer) (Hemiptera: Aphididae), is a major pest worldwide. The intensive use of insecticides has led to the development of resistance against neonicotinoid insecticides. The R81T mutation in the nicotinic acetylcholine receptor (nAChR) beta1 subunit is considered a crucial mechanism adaptation to neonicotinoid resistance in M. persicae and Aphis gossypii. Resistance-related mutations (R81T and V101I) were detected in the imidacloprid-resistant M. persicae AH19 population. The V101I mutation is reported for the first time. The V101I and R81T mutations existed separately, indicating that the two mutations evolved independently. Imidacloprid resistance in the AH19 population was stable without insecticide exposure. Four mutant strains were selected from the population with stable resistance. The resistance of the AH19-T, AH19-I, and AH19-TI strains to imidacloprid, thiamethoxam, and dinotefuran was significantly increased compared with the AH19-W strain. Synergism bioassays showed that the inhibition of three detoxification enzymes did not affect imidacloprid resistance in the AH19-T and AH19-I strains. Expression of nAChR β1 subunits in the AH19-W, AH19-T, and AH19-I strains remained unchanged. The V101I mutation is associated with neonicotinoid resistance in M. persicae. The resistance of the AH19-T and AH19-I strains to neonicotinoids appears to be mainly due to the R81T and V101I mutations, whereas these mutations, together with changes in the cytochrome P450 monooxygenases and nAChR expression may be responsible for the development of neonicotinoid resistance in the AH19-TI strain. © 2021 Society of Chemical Industry.