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 F1 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.

A link between host plant adaptation and pesticide resistance in the polyphagous spider miteTetranychus urticae

“…The strain was controlled by regular foliar applications of commercial formulations of the following acaricides: tebufenpyrad, pyridaben, clofentezine, hexythiazox, bifenthrin, fenbutatin oxide, abamectine, and oxamyl. Resistance to mitochondrial electron transport inhibitor (METI) acaricides is well characterized in MR-VP (104). The Marathonas (MAR-AB) strain was isolated from a heavily sprayed rose greenhouse near Athens (Greece) in 2009.…”

Acaricides - Biological Profiles, Effects and Uses in Modern Crop Protection

“…This acaricide, launched in 1998, is usually classified among mite growth inhibitors, together with clofentezine and hexythiazox, older acaricides that cause similar symptoms (Marčić, 2003;Krämer & Schirmer, 2007), but whose exact mode of action is unknown. On the other hand, Nauen & Smagghe (2006) Marčić, 2007;Marčić et al, 2007;Van Pottelberge et al, 2009;Marčić et al, 2010). These two acaricides are the only new compounds used for control of eriophyoid mites as well .…”

“…The insensivity of acetylcholinesterase is the most common type of organophosphorous resistance in T. urticae (Cranham & Helle, 1985;, Tsagkarakou et al, 2002Khajehali et al, 2010;Kwon et al, 2010a). Metabolic resistance mediated by carboxylesterases was found in majority of cases of resistance development to pyrethroids in this species (Ay & Gűrkan, 2005;van Leeuwen et al, 2005b, while the oxidative metabolism appears to play a major role in resistance to METI-acaricides Kim et al, 2004Kim et al, , 2006van Pottelberge et al, 2009). The results of numerous conventional genetic studies indicate that in most cases single major gene controls inheritance of resistance in spider mites (Cranham & Helle, 1985;.…”

Control of the Two-Spotted Spider Mite, Tetranychus urticae Koch on Kidney Bean and Pea Plants

“…It has been estimated that the spider mite, T. urticae has evolved resistance to more than 80 acaricides to date (Knowles, 1997;Devine et al, 2001;Choi et al, 2004;Van Pottelberge et al, 2008 and) and resistance has been reported from many countries. As for mechanisms of resistance to acaricides with new modes of action (e.g.…”

“…As for mechanisms of resistance to acaricides with new modes of action (e.g. Abamectin, fenpyroximate, chlorphenapyr, METI-acaricides, spirodiclofen) enhanced detoxification in T. urticae strains has been reported (Devine et al, 2001;Nauen 2001and 2002;Kim et al, 2004a and b;Van Leeuwen et al, 2006;Van Pottelberge et al, 2008 and). …”