Search

Tetranychus urticae Koch (T. urticae) is one of the most tremendous herbivores due to its polyphagous characteristics, and is resistant to most acaricides. In this study, enzyme-linked immunosorbent assay (ELISA), transcriptome sequencing (RNA-seq) and quantitative real-time PCR (qRT-PCR) were carried out to analyze the mechanisms of T. urticae metabolic resistance to cyflumetofen and bifenthrin on cowpea. The enzyme activity of UDP-glucuronosyltransferases (UGTs) and carboxylesterases (CarEs) in the cyflumetofen-resistant (R_cfm) strain significantly decreased, while that of cytochrome P450 monooxygenases (P450s) significantly increased. Meanwhile, the activities of glutathione-S-transferases (GSTs), CarEs and P450s in the bifenthrin-resistant (R_bft) strain were significantly higher than those in the susceptible strain (Lab_SS). According to the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses, in the R_cfm mite strain, two carboxyl/cholinesterase (CCE) genes and two P450 genes were upregulated and one gene was downregulated, namely CYP392E7; in the R_bft mite strain, eleven CCE, nine UGT, two P450, four GST and three ABC genes were upregulated, while four CCE and three P450 genes were downregulated. Additionally, 94 differentially expressed genes (DEGs) were common to the two resistant groups. Specifically, TuCCE46 and TuCCE70 were upregulated in both resistant groups. Furthermore, the qRT-PCR validation data were consistent with those from the transcriptome sequencing analysis. Specifically, TuCCE46 (3.37-fold) was significantly upregulated in the R_cfm strain, while in the R_bft strain, TeturUGT22 (5.29-fold), teturUGT58p (1.74-fold), CYP392A11 (2.89-fold) and TuGSTd15 (5.12-fold) were significantly upregulated and TuCCE01 (0.13-fold) and CYP392A2p (0.07-fold) were significantly downregulated. Our study indicates that TuCCE46 might play the most important role in resistance to cyflumetofen, and TuCCE01, teturUGT58p, teturUGT22, CYP392A11, TuGSTd15, TuGSTm09 and TuABCG-13 were prominent in the resistance to bifenthrin. These findings provide further insight into the critical genes involved in the metabolic resistance of T. urticae to cyflumetofen and bifenthrin. [ABSTRACT FROM AUTHOR]

BACKGROUND: Tetranychus urticae (T. urticae) Koch is an important pest of vegetable crops worldwide. In this study, bioassays were carried out to analyze the resistance risk, multi‐resistance and management of T. urticae Koch to bifenthrin, bifenazate and cyflumetofen on cowpea. RESULTS: The resistance ratios of the adult T. urticae population to bifenthrin (G16), bifenazate (G12) and cyflumetofen (G12) were 31.29, 9.38 and 5.81, respectively. Realized heritability (h2) analysis showed that, under a selection pressure of 50–90% mortality, the generations needed to increase 10‐fold LC50 values of bifenthrin, bifenazate and cyflumetofen were 3.64–8.05, 5.75–12.71, and 10.93–24.15, respectively. No obvious multi‐resistance among these three acaricides was observed. Synergist bioassay results showed that microsomal multifunctional oxidase (MFO) was involved in bifenthrin resistance of T. urticae, with a synergistic ratio of 22.38. However, MFO and GSTs were not the main factors conferring the resistance to bifenazate. MFO, glutathione S‐transferases(GSTs), together with esterase contributed to the development of the resistance to cyflumetofen. Additionally, the toxicity selection index test showed that bifenazate was safe to the natural enemy Neoseiulus barkeri (N. barkeri) with a toxicity selection index (TSI) >484.85, while bifenthrin was the least safe (TSI = 0.92). CONCLUSIONS: These results demonstrated the T. urticae developed higher resistance risk to bifenthrin compared to bifenazate and cyflumetofen and no obvious multi‐resistance among these three acaricides, providing guidance for designing appropriate strategies for the effective application of bifenthrin, bifenazate and cyflumetofen in the field and delaying the development of insecticide resistance. © 2019 Society of Chemical Industry [ABSTRACT FROM AUTHOR]