Resistance mechanisms to mitochondrial electron transport inhibitors in a field-collected strain ofTetranychus urticaeKoch (Acari: Tetranychidae)

Abstract A Belgian field strain (MR-VP) of Tetranychus urticae (Koch) (Acari: Tetranychidae) exhibits different levels of resistance to four frequently used METI (mitochondrial electron transport inhibitor)-acaricides, i.e. tebufenpyrad, fenpyroximate, pyridaben and fenazaquin. Resistance factors for these compounds were 184, 1547, 5971 and 35, respectively. A 23.5-fold increase in 7-ethoxy-4-trifluoromethylcoumarin O -deethylation activity suggested that metabolic resistance through elevated levels of cytochrome P450 dependent monooxygenase-activity is a possible resistance mechanism. However, synergism studies with different metabolic inhibitors revealed some contrasting resistance mechanisms between the METI-acaricides. Tebufenpyrad resistance could only be synergized after pre-treatment with the monooxygenase inhibitor piperonyl butoxide (PBO), whereas pyridaben resistance was strongly synergized both by PBO and the esterase inhibitor S,S,S-tributylphosphorotrithioate (DEF). Resistance levels to fenpyroximate could neither be suppressed by PBO nor by DEF. Although METI-acaricides are structurally related, these findings probably reflect a different role of esterases and mono-oxygenases in metabolic detoxification between these compounds. The overall lack of synergism by diethylmaleate (DEM) suggests that glutathione- S -transferases are not an important factor in resistance to METIs. Reciprocal crosses between susceptible females and resistant males showed no maternal effect, and resistance to METI-acaricides was inherited generally as a dominant trait. Backcrosses with F 1 females revealed striking differences in the mode of inheritance. Although resistance to fenpyroximate and pyridaben was under monogenic control, resistance to tebufenpyrad was under control of more than one gene.