Abstract

AbstractThe small brown planthopper (SBPH), Laodelphax striatellus (Fallén), is an important pest of rice that has developed resistance and even cross‐resistance to insecticides. In a previous study, we found that the resistance mechanism of a deltamethrin‐resistant strain of SBPH (JH‐del) involved the enhancement of detoxification enzyme activity and was unrelated to target resistance. The JH‐del strain exhibited cross‐resistance to fenvalerate. To explore the detoxification enzymes responsible for cross‐resistance to pyrethroids in the SBPH, quantitative real‐time PCR, transgenic Drosophila technology, the GAL4/UAS system and inhibition assays of recombinantly expressed P450s were carried out. Transgenic Drosophila strains da > CYP4FB1 and da > CYP301B1 overexpressing SBPH CYP4FB1 and CYP301B1 showed significantly increased resistance to deltamethrin, fenvalerate and etofenprox. CYP4FB1 and CYP301B1 were overexpressed by 3.41‐ and 4.99‐fold, respectively, in the JH‐del strain. Recombinant CYP4FB1 and CYP301B1 showed good O‐demethylation and O‐deethylation activities on p‐nitroanisole (PNA) and 7‐ethoxycoumarin (EC), respectively. The half‐maximal inhibitory concentrations (IC50) of deltamethrin, fenvalerate and etofenprox on recombinant CYP4FB1 and CYP301B1 were 0.15–1.35 μM, while those of chlorpyrifos and imidacloprid against recombinant CYP4FB1 and CYP301B1 were 6.99–15.91 μM. Therefore, recombinant CYP4FB1 and CYP301B1 have a strong affinity for pyrethroids and a weak binding ability to other types of insecticides. In summary, CYP4FB1 and CYP301B1 are the detoxification enzymes that mediate the cross‐resistance of the JH‐del strain to three pyrethroids. The results revealed the cross‐resistance mechanism of SBPH to pyrethroids and provided a theoretical basis for the resistance management of SBPH.

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