Sibel Yorulmaz Salman

Etoxazole resistance in predatory mite Phytoseiulus persimilis A.-H. (Acari: Phytoseiidae): Cross-resistance, inheritance and biochemical resistance mechanisms.

Phytoseiulus persimilis of the family Phytoseiidae is an effective predatory mite species that is used to control pest mites. The LC50 and LC60 values of etoxazole were determined on P. persimilis using a leaf-disc method and spraying tower. A laboratory selection population designated ETO6 was found to have a 111.63-fold resistance to etoxazole following 6 selection cycles. This population developed low cross-resistance to spinosad, spiromesifen, acetamiprid, indoxacarb, chlorantraniliprole, milbemectin and moderate cross-resistance to deltamethrin. PBO, IBP and DEM synergised resistance 3.17-, 2.85- and 3.60-fold respectively. Crossing experiments revealed that etoxazole resistance in the ETO6 population was an intermediately dominant and polygenic. In addition, detoxifying enzyme activities were increased 2.71-fold for esterase, 3.09-fold for glutathione S-transferase (GST) and 2.76-fold for cytochrome P450 monooxygenase (P450) in the ETO6 population. Selection for etoxazole under laboratory conditions resulted in the development of etoxazole resistance in the predatory mite P. persimilis that are resistant to pesticides are considered valuable for use in resistance management programmes within integrated pest control strategies.

Acequinocyl resistance in Tetranychus urticae Koch (Acari: Tetranychidae): inheritance, synergists, cross-resistance and biochemical resistance mechanisms

Acequinocyl is the only commercialized acaricide of the naphthoquinone analogue group. To develop strategies to minimize resistance, a laboratory-selected acequinocyl-resistant strain of the two-spotted spider mite Tetranychus urticae was used to determine the inheritance, toxicological, biochemical and cross-resistance data. The LC50 and LC60 values of acequinocyl were determined on T. urticae using a leaf-disc method and spraying tower. A laboratory selection population designated ACE6 had a122.0-fold resistance to acequinocyl following six selection cycles. A selected strain showing 112.0-fold resistance was named ACE6 population. This population developed low resistance to etoxazole and spirodiclofen and moderate cross-resistance to hexythiazox, milbemectin and bifenazate. Monooxygenase enzyme inhibitor piperonyl butoxide, the esterase enzyme inhibitor S-benzyl O,O-diisopropyl phosphorothioate and the glutathione S-transferase (GST) enzyme inhibitor diethyl maleate synergized resistance values were 1.0-, 2.5- and ˂1-fold, respectively. Crossing experiments revealed that acequinocyl resistance in the ACE6 population was intermediately dominant and monogenic. In addition, the detoxifying enzyme activities were increased 3.03-fold for esterase, ˂1-fold for GST and 1.00-fold for cytochrome P450 monooxygenase in the ACE6 population. The results suggest that esterase enzyme may play a role in acequinocyl resistance, while the GST and P450 enzymes do not appear to have any significant involvement.