Effects of mutations in Drosophila nicotinic acetylcholine receptor subunits on sensitivity to insecticides targeting nicotinic acetylcholine receptors.

摘要

Several strains of Drosophila melanogaster possess mutant alleles in nicotinic acetylcholine receptor (nAChR) subunits, D alpha 1 and D beta 2 that confer resistance to neonicotinoids such as imidacloprid and nitenpyram, and D alpha 6, that confers resistance to spinosyns. These mutant strains were bioassayed with a selected set of nAChR active insecticides including neonicotinoids, spinosad, and sulfoxaflor, a new sulfoximine insecticide. All of the neonicotinoids examined, except dinotefuran showed reduced insecticidal efficacy on larvae of the D alpha 1 mutant, suggesting that this subunit may be important in the action of these insecticides. All of the neonicotinoids, including dinotefuran, showed reduced insecticidal efficacy on larvae possessing the D beta 2 mutation. A similar pattern of broad neonicotinoid resistance to that of D beta 2 alone was also observed for larvae with both the mutations (D alpha 1+D beta 2). The D beta 2 mutation exhibited a lower level of cross-resistance to sulfoxaflor (<3-fold) than to any of the neonicotinoids (>13-fold). In contrast, there was no cross-resistance for any of the neonicotinoids or sulfoxaflor in adult flies with the D alpha 6 mutation, which confers high levels of resistance to spinosad. Thus in the D. melanogaster strains studied, target site resistance observed for the neonicotinoids and the spinosyns does not translate directly to resistance towards sulfoxaflor.