Background: Information about genetic and biochemical mechanisms of arthropods resistance to pesticide obtained with resistant and susceptible genotypes is more correct than that of population-based samples. Materials and methods: The disruptively selection of two-spotted spider mites was carried out on the basis of the presence or absence of resistance to four acaricides - dimethoate, bifenthrin, abamectin and bromopropylate. A possible resistance mechanisms of mite to abamectin and bromopropylate was detected when testing the diagnostic` concentrations of acaricides which toxic action is known. Synergetic effect of resistant genotypes treated with monooxygenase inhibitor piperonyl butoxide (PBO) was studied. Carboxylesterase isoenzymes were determined with use of poliacrylamide gel electrophoresis in individual genotypes of spider mite. Results: Statistical analysis of genotypes selection results demonstrated 30 % of females with no traits of resistance to the toxicant in all resistant lines of each generation. The reason this is arrhenotokous reproduction spider mites and dominant status of alleles determining the traits of resistance. Abamectin and bromopropylate resistant mites were synergized by PBO. Resistance was positively correlated with increased carboxylesterase activity in resistant genotypes. Conclusion: Reduced sensitivity to pesticides in resistant arthropods was found in alteration recordings sensory receptivity and through elevated levels of carboxylesterase and monooxygenase activity. This is universal adaptive response of the arthropods organism to intoxication by any pesticides.
Background. The presence in interline hybrids two-spotted spider mite Tetranychus urticae Koch two genes determining resistance to acaricides of various chemical classes significantly increases their sensitivity to the action of each these toxicants. Materials and methods. The resistant and susceptible to malathion, bifenthrin and abamectin inbred lines of spider mite by disruptive selection cycles were obtained. The toxicological tests were performed by diagnostic concentrations of acaricides. The protein marker gene of resistance to malathion was determined by poliacrylamide disc-electrophoresis. Results. The epistatic interaction of resistance genes to different acaricides is not manifestation at the stages of transcription and translation of genetic information. Conclusion. The epistatic effect of another gene on the resistance gene to the current acaricide is a different consequence of metabolism processes encoded by each gene at the stage of phenotypic regulation.
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