Differential metabolism of imidacloprid and dinotefuran by Bemisia tabaci CYP6CM1 variants

• Published in: Pesticide biochemistry and physiology Vol. 159; pp. 27 - 33
• Main Authors: Hamada, Akira, Wahl, Gregory D., Nesterov, Alexandre, Nakao, Toshifumi, Kawashima, Miyuki, Banba, Shinichi
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.09.2019
• Subjects: Animals; Bemisia tabaci; CYP6CM1; Dinotefuran; Guanidines - metabolism; Guanidines - pharmacology; Hemiptera - drug effects; Hemiptera - genetics; Hemiptera - metabolism; Imidacloprid resistance; Insect Proteins - genetics; Insect Proteins - metabolism; Insecticide Resistance - genetics; Insecticides - metabolism; Insecticides - pharmacology; Neonicotinoids; Neonicotinoids - metabolism; Neonicotinoids - pharmacology; Nitro Compounds - metabolism; Nitro Compounds - pharmacology; Triazines - metabolism; Triazines - pharmacology; Dinotefuran; Neonicotinoids; CYP6CM1; Bemisia tabaci; Imidacloprid resistance
• ISSN: 0048-3575; 1095-9939
• DOI: 10.1016/j.pestbp.2019.05.011

Imidacloprid has been used to control one of most serious pests, Bemisia tabaci. However, B. tabaci has developed imidacloprid resistance mainly by over-expressing CYP6CM1. It was reported that imidacloprid-resistant B. tabaci showed no or low level of cross-resistance against dinotefuran. Here, we expressed CYP6CM1 variants using Sf9/baculovirus and/or Drosophila S2 cells and showed that CYP6CM1 variants metabolized imidacloprid but not dinotefuran. In addition, we demonstrated that imidacloprid and pymetrozine competed for a CYP6CM1 variant more efficiently than dinotefuran, using a luminescent substrate competition assay. These results suggest that lack of metabolic activity of CYP6CM1 variants against dinotefuran caused no or low level of cross-resistance. [Display omitted] •Bemisia tabaci has developed imidacloprid resistance by over-expressing CYP6CM1.•CYP6CM1 variants metabolized imidacloprid, but did not dinotefuran.•Imidacloprid competed with luminescent substrate for CYP6CM1 more efficiently than dinotefuran.•Lack of metabolism by CYP6CM1 variants against dinotefuran caused no or low cross-resistance.