Background: Mitochondrial Electron Transport Inhibitors of complex I (METI-I), such as tebufenpyrad and fenpyroximate, are acaricides that have been used extensively to control Tetranychus urticae Koch (Acari: Tetranychidae) for more than 20 years. Because of the ability of this spider mite to rapidly develop acaricide resistance, field (cross-) resistance monitoring and elucidation of resistance mechanisms are extremely important for resistance management (RM). In the present study, 42 European T. urticae field populations were screened for tebufenpyrad and fenpyroximate resistance, and the correlation between resistance and the H92R substitution in PSST was investigated.
Results: According to the calculated lethal concentration values that kill 90% of the population (LC90 ), tebufenpyrad and fenpyroximate would fail to control many of the collected populations at recommended field rates. Six populations exhibited high to very high resistance levels (200- to over 1950-fold) to both METI-Is. Analysis based on the LC50 values displayed a clear correlation between tebufenpyrad and fenpyroximate resistance, further supporting cross-resistance, which is of great operational importance in acaricide RM. The previously uncovered METI-I target-site mutation H92R in the PSST homologue of complex I (NADH:ubiquinone oxidoreductase) was found with high allele frequencies in populations resistant to tebufenpyrad and fenpyroximate. Synergist assays showed this mutation is not the only factor involved in METI-I resistance and additive or synergistic effects of multiple mechanisms most likely determine the phenotypic strength.
Conclusions: The predictive value of resistance by H92R is very high in European populations and offers great potential to be used as a molecular diagnostic marker for METI-I resistance. © 2022 Society of Chemical Industry.
Keywords: METI-I acaricides; Tetranychus urticae; cross-resistance; molecular marker; resistance management.
© 2022 Society of Chemical Industry.