부산대학교 도서관

Neonicotinoid insecticides, which target insect nicotinic acetylcholine receptors (nAChRs), have been widely and intensively used to control the whitefly, Bemisia tabaci, a highly damaging, globally distributed, crop pest. This has inevitably led to the emergence of populations with resistance to neonicotinoids. However, to date, there have been no reports of target-site resistance involving mutation of B. tabaci nAChR genes. Here we characterize the nAChR subunit gene family of B. tabaci and identify dual mutations (A58T&R79E) in one of these genes (BTβ1) that confer resistance to multiple neonicotinoids. Transgenic D. melanogaster, where the native nAChR Dβ1 was replaced with BTβ1A58T&R79E, were significantly more resistant to neonicotinoids than flies where Dβ1 were replaced with the wildtype BTβ1 sequence, demonstrating the causal role of the mutations in resistance. The two mutations identified in this study replace two amino acids that are highly conserved in >200 insect species. Three-dimensional modelling suggests a molecular mechanism for this resistance, whereby A58T forms a hydrogen bond with the R79E side chain, which positions its negatively-charged carboxylate group to electrostatically repulse a neonicotinoid at the orthosteric site. Together these findings describe the first case of target-site resistance to neonicotinoids in B. tabaci and provide insight into the molecular determinants of neonicotinoid binding and selectivity. Author summary: The sweet potato whitefly, Bemisia tabaci, is an important target pest of neonicotinoid insecticides. Much is known about the neonicotinoid-resistance evolved in whitefly by over-expressed detoxifying enzymes. But the toxicological targets of neonicotinoids, the nAChR subunit genes in whitefly are less well understood. In this study, we characterized the nAChR subunit gene family of whitefly, and identified dual mutations in beta1 subunit that confer resistance to multiple neonicotinoid insecticides. These findings are significant as they demonstrate how resistance can arise as a result of mutations in insects that had a combined effect to repulse the insecticides thus overcoming the insect selectivity of an important class of insecticides. [ABSTRACT FROM AUTHOR]