Stability, cross‐resistance, mechanisms and inheritance of laboratory‐selected resistance to chlorfenapyr in Plutella xylostella

BACKGROUND The diamondback moth (DBM), Plutella xylostella (Linnaeus), a globally destructive pest of cruciferous crops, has developed resistance to numerous insecticides, including chlorfenapyr. To elucidate the resistance characteristics of DBM to chlorfenapyr, a resistant strain was selected from a susceptible strain in the laboratory, and its resistance inheritance, cross‐resistance spectrum and potential mechanisms were investigated. RESULTS Intermittent laboratory selection showed that chlorfenapyr resistance was unstable, increasing with continuous selection but declining in its absence. At the 106th generation, the resistant strain exhibited 110.03‐fold resistance to chlorfenapyr, with very low cross‐resistance (2.05‐ to 3.22‐fold) to tolfenpyrad, spinosad, abamectin, diafenthiuron and chlorantraniliprole, and no cross‐resistance to emamectin benzoate, lufenuron, pyridalyl, indoxacarb and metaflumizone. Genetic analyses uncovered that the resistance to chlorfenapyr was inherited as autosomal, incompletely dominant, and polygenic trait. Synergistic bioassays revealed that the esterase inhibitors DEF and TPP, glutathione S‐transferase (GST) inhibitor DEM and cytochrome P450 monooxygenase (P450) inhibitor PBO all significantly synergized the chlorfenapyr toxicity in this resistant strain, with synergism ratios of 3.85, 3.55, 2.55 and 1.85, respectively, but had no such effect on the susceptible strain. CONCLUSION Laboratory‐selected chlorfenapyr resistance in DBM is unstable, follows an autosomal, incompletely dominant, and polygenic mode of inheritance, is mediated by enhanced detoxification, and shows no or very low cross resistance to other tested insecticides.