LAUSR

Insecticide resistance is one of the major obstacles for controlling agricultural pests. There have been a lot of studies on insecticides stimulating the development of insect resistance. Herbicides account for the largest sector in the agrochemical market and are often co-applied with insecticides to control insect pests and weeds in the same cropland ecosystem. However, whether and how herbicides exposure will affect insecticide resistance in insect pests is largely unexplored. Here we reported that after exposure to herbicide butachlor, the lepidopteran Spodoptera litura larvae reduced susceptibility to the insecticide chlorpyrifos. Docking simulation studies suggested that general odorant-binding protein 2 (GOBP2) could bind to butachlor with high binding affinity, and silencing SlGOBP2 by RNA interference (RNAi) decreased larval tolerance to chlorpyrifos. Butachlor exposure induced ecdysone biosynthesis, whose function on increasing chlorpyrifos tolerance was supported in synergism experiments and confirmed by silencing the key gene (SlCYP307A1) for ecdysone synthesis. Butachlor exposure also activated the expression of detoxification enzyme genes. Silencing the genes with the highest herbicide-induced expression among the three detoxification enzyme genes led to increased larval susceptibility to chlorpyrifos. Collectively, we proposed a new mechanism that olfactory recognition of herbicides by GOBP2 triggers insect hormone biosynthesis and leads to high metabolic tolerance against insecticides. These findings provide valuable information for the dissection of mechanisms of herbicide-induced resistance to insecticides and also supplements the development of reduced-risk strategies for pest control.