Differential metabolism of neonicotinoids by brown planthopper, Nilaparvata lugens, CYP6ER1 variants

• Published in: Pesticide biochemistry and physiology Vol. 165; p. 104538
• Main Authors: Hamada, Akira, Stam, Lynn, Nakao, Toshifumi, Kawashima, Miyuki, Banba, Shinichi
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.05.2020
• Subjects: Animals; CYP6ER1; Dinotefuran; Hemiptera; Imidacloprid resistance; Insecticide Resistance; Insecticides; Neonicotinoids; Nilaparvata lugens; Nitro Compounds; RR; CPR; Imidacloprid resistance; Neonicotinoids; IRAC; MRM; CYP6ER1; RME; p-NP; Dinotefuran; ECOD; REE; RBE; BFCOD; Nilaparvata lugens; APRD
• ISSN: 0048-3575; 1095-9939
• DOI: 10.1016/j.pestbp.2020.02.004

Imidacloprid is very effective in controlling Nilaparvata lugens Stål, which severely damages rice plants. Following heavy imidacloprid use, imidacloprid-resistant N. lugens, which showed cross-resistance to other neonicotinoids, appeared. We used the baculovirus/Sf9 expression system to express CYP6ER1 variants carrying A375del + A376G (del3) mutations, either with or without T318S mutation, which confer imidacloprid resistance in N. lugens. These CYP6ER1 variants metabolized imidacloprid but did not metabolize dinotefuran. Moreover, Drosophila expressing a CYP6ER1 variant carrying T318S + del3 mutations were resistant to imidacloprid, with a resistance ratio of 288.7, whereas the resistance ratio to dinotefuran was 3.6. These findings indicate that N. lugens has a low level of resistance to dinotefuran, and the increase of resistance is slow. We also studied the metabolism of other neonicotinoids, as well as sulfoxaflor and flupyradifurone, by CYP6ER1 variants carrying del3 mutations, either with or without the T318S mutation. Sulfoxaflor, was not metabolized by either CYP6ER1-del3 or CYP6ER1-T318Sdel3 variants. However, these variants did metabolize flupyradifurone. This study sheds light on the substrate selectivity of CYP6ER1 variants. [Display omitted] •N. lugens has developed imidacloprid (IMI) resistance by over-expressing CYP6ER1 variants.•CYP6ER1 variants metabolized IMI, but not dinotefuran (DTF).•Drosophila over-expressing the CYP6ER1 variant were resistant to IMI, but much less so to DTF.•Lack of metabolism by CYP6ER1 variants against DTF resulted in low cross-resistance.