Changes in insecticide susceptibilities and detoxifying enzyme activities were measured in a strain of Tetranychus urticae Koch following repeated exposure to the organophosphate insecticide, chlorpyrifos. Twelve consecutive selection at the LC 60 of the parental strain increased resistance from 8.58 to 91.45 fold. The interaction of some synergists [piperonyl butoxide, triphenyl phosphate and S-benzyl-O,O-diisopropyl phosphorothioate (IBP)] with chlorpyrifos was analyzed in the selected strain. Solely IBP showed a low synergistic effect with chlorpyrifos. The selected strain also demonstrated resistance against abamectin, propargite, clofentezine and fenpyroximate. The mode of resistance inheritance to chlorpyrifos was found to be incompletely dominant, and not sex-linked. Non-specific esterase enzyme activity was raised from 19.35 to 33.59 mOD/min/mg proteins during the selection period and it was observed that esterase band intensities visualized by polyacrylamide gel electrophoresis increased. This study has investigated the selection of resistance to chlorpyrifos and documented resistance to abamectin, propargite, clofentezine and fenpyroximate in Turkish T. urticae. Esterase enzymes may be playing a role in chlorpyrifos resistance while glutathione S-transferase (GST) and P450 enzymes do not appear to have any significant involvement.

No abstract

No abstract

No abstract

Myzus persicae (Sulzer) (Hemiptera: Aphididae) is a polyphagous pest that causes significant losses in many crops. In the present study, the biochemical and molecular mechanism of acetamiprid resistance in a laboratory-selected Myzus persicae population of which the resistance ratios reached 57.5-fold were investigated. This study was conducted in the Isparta University of Applied Sciences, Agriculture Faculty, Department of Plant Protection in 2018 and 2020. Synergism, biochemical and molecular assays showed the absence of increased P450 activity in selected population. In addition, no point mutation in nicotinic acetylcholine receptor (nAChR), the target-site of neonicotinoids including acetamiprid, was detected in the selected population. These results suggests that high level of acetamiprid resistance might be developed via the mechanisms other than well-known mechanisms, such as increased P450 activity and target-site mutations. The population selected with acetamiprid showed decreased susceptibility to imidacloprid, sulfaxaflor, beta-cyfluthrin, and tau-fluvanite ranging from 1.54 to 4.76. Nonetheless, more studies are needed to support cross-resistance by Myzus persicae populations having different genetic backgrounds.