Pyriproxyfen resistance of Bemisia tabaci (Homoptera: Aleyrodidae) biotype B: metabolic mechanism.

Juvenile hormone (JH) analog insecticides are relatively nontoxic to vertebrates and provide efficient control of key arthropod pests. One JH analog, pyriproxyfen, has provided over a decade of exceptional management of whiteflies in cotton of the southwestern United States. Thwarting resistance to pyriproxyfen in Bemisia tabaci (Gannadius) (a.k.a. Bemisia argentifolii Bellows and Perring) has been the focus of an integrated resistance management program because this insecticide was first registered for use in Arizona cotton in 1996. Resistance levels have increased slowly in field populations in recent years but have not demonstrably affected field performance of pyriproxyfen. Resistant strains have been isolated and studied in the laboratory to determine the mechanism of resistance and identify optimal strategies for controlling resistant whiteflies. Synergism bioassays showed that resistance in a laboratory-selected strain QC02-R, was partially suppressible with piperonyl butoxid (PBO) and diethyl maleate (DEM) but not with S, S, S-tributyl phosphorotrithioate (DEF). Consistent with the synergism bioassay results, enzymatic assays revealed that the enzyme activities of cytochrome P450 monooxygenases (P450) and glutathione S-transferases (GST) but not esterases were significantly higher in the pyriproxyfen-resistant QC02-R strain than in the susceptible strain. These results indicate that both P450 and GST are involved in whitefly resistance to pyriproxyfen.