Target-Site Mutations and Glutathione S-Transferases Are Associated with Acequinocyl and Pyridaben Resistance in the Two-Spotted Spider Mite Tetranychus urticae (Acari: Tetranychidae).

Jihye Choi,Sung Il Kim,Hyunkyung Kim,Bueyong Park,Hyun-Na Koo,Gil-Hah Kim

doi:10.3390/insects11080511

Abstract

Simple SummaryThe two-spotted spider mite Tetranychus urticae is a difficult-to-control pest due to its short life cycle and rapid resistance development. In this study, we characterized field strains collected in 2001 and 2003 that have been selected for acequinocyl resistance and pyridaben resistance, respectively. These strains displayed resistance ratios of 1798.6 and 5555.6, respectively, and were screened for cross-resistance against several currently used acaricides. The acequinocyl resistant strain exhibited pyridaben cross-resistance, but the pyridaben resistant strain showed no cross-resistance. The acequinocyl resistant strain exhibited point mutations in cytb (I256V and N321S) and PSST (H92R). In contrast, the pyridaben resistant strain exhibited the H92R but not the I256V and N321S point mutations. In addition, the increased GST metabolism and GST delta expression might be related to acequinocyl resistance in Tetranychus urticae. We hope that the data and patterns described here can now be exploited in the continued quest for rational resistance management strategies.The two-spotted spider mite Tetranychus urticae is a difficult-to-control pest due to its short life cycle and rapid resistance development. In this study, we characterized field strains collected in 2001 and 2003 that were selected for acequinocyl resistance (AR) and pyridaben resistance (PR), respectively. These strains displayed resistance ratios of 1798.6 (susceptible vs. AR) and 5555.6 (susceptible vs. PR), respectively, and were screened for cross-resistance against several currently used acaricides. The AR strain exhibited pyridaben cross-resistance, but the PR strain showed no cross-resistance. The AR strain exhibited point mutations in cytb (I256V, N321S) and PSST (H92R). In contrast, the PR strain exhibited the H92R but not the I256V and N321S point mutations. In some cases increased glutathione S-transferase (GST) activity has previously been linked to enhanced detoxification. The AR strain exhibited approximately 2.3-, 1.8-, and 2.2-fold increased GST activity against 1-chloro-2,4-dinitrobenzene (CDNB), 1,2-dichloro-4-nitrobenzene (DCNB), and 4-nitrobenzyl chloride (NBC), respectively. Among the five GST subclass genes (delta, omega, mu, zeta, and kappa), the relative expression of delta class GSTs in the AR strain were significantly higher than the PR and susceptible strain. These results suggest that the I256V and N321S mutations and the increased GST metabolism and GST delta overexpression might be related to acequinocyl resistance in T. urticae.

Highlights

The two-spotted spider mite Tetranychus urticae Koch (Arthropoda: Acari: Tetranychidae) is a worldwide agricultural pest that invades a wide range of host crops
These results suggest that the I256V and N321S mutations and the increased glutathione S-transferase (GST) metabolism and GST delta overexpression might be related to acequinocyl resistance in T. urticae
The G126S + A133T point mutations were detected in field-collected populations of T. urticae, but the I256V + N321S point mutations were not found. These findings suggest that alternative mechanisms are in place, possibly including increased metabolism, as was previously reported

Summary

Introduction

The two-spotted spider mite Tetranychus urticae Koch (Arthropoda: Acari: Tetranychidae) is a worldwide agricultural pest that invades a wide range of host crops. Tetranychus urticae is likely to develop acaricide resistance faster than other pests, and there have been reports on its development of resistance to almost all types of acaricides currently registered [5,6]. Acequinocyl is a naphthoquinone compound discovered in the 1970s by DuPont [7]. It is a proacaricide that breaks down into the active metabolite, a deacetylated product. A mechanistic study showed that the deacetylated metabolite of acequinocyl inhibits respiration in mitochondria at the ubiquinol oxidation site (Q0 ) of complex III of the electron transfer chain [8,9,10]. Pyridaben is a novel pyridazine compound discovered in 1984 by Nissan

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