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Ralf Nauen – 1st expert on this subject based on the ideXlab platform
Abamectin is metabolized by cyp392a16 a cytochrome p450 associated with high levels of acaricide resistance in tetranychus urticaeInsect Biochemistry and Molecular Biology, 2014Co-Authors: Maria Riga, T G Van Leeuwen, Dimitra Tsakireli, Aris Ilias, Evangelia Morou, Antonis Myridakis, Euripides G Stephanou, Ralf Nauen, Wannes DermauwAbstract:
Abstract Abamectin is one of the most important insecticides worldwide. It is used against major agricultural pests and insects of public health importance, as well as against endoparasites in animal health. Abamectin has been used successfully for the control of the spider mite Tetranychus urticae , a major agricultural pest with global distribution, an extremely diverse host range, and a remarkable ability to develop resistance against insecticides including Abamectin. Target site resistance mutations may explain a large part of resistance, although genetic evidence and transcriptomic data indicated that additional mechanisms may also be implicated in the Abamectin resistant phenotype. To investigate a functional link between cytochrome P450-mediated metabolism and Abamectin resistance, we recombinantly expressed three cytochrome P450s (CYP392A16, CYP392D8 and CYP392D10) that have been associated with high levels of Abamectin resistance in a resistant T. urticae strain isolated from Greece. CYP392A16 was expressed predominately in its P450 form however, both CYP392D8 and CYP392D10 were expressed predominately as P420, despite optimization efforts on expression conditions. CYP392A16 catalyses the hydroxylation of Abamectin ( K cat = 0.54 pmol/min/pmol P450; K m = 45.9 μM), resulting in a substantially less toxic compound as confirmed by bioassays with the partially purified metabolite. However, CYP392A16 did not metabolize hexythiazox, clofentezine and bifenthrin, active ingredients that also showed reduced toxicity in the Abamectin resistant strain. Among a number of fluorescent and luminescent substrates screened, Luciferin-ME EGE was preferentially metabolized by CYP392A16, and it may be a potential diagnostic probe for metabolic resistance detection and monitoring.
biochemical markers linked to Abamectin resistance in tetranychus urticae acari tetranychidaePesticide Biochemistry and Physiology, 2002Co-Authors: Natascha Stumpf, Ralf NauenAbstract:
Abstract Abamectin resistance monitoring with the two-spotted spider mite, Tetranychus urticae Koch, using a diagnostic dose revealed resistant strains from the Netherlands (NL-00), Colombia (COL-00), and Brazil (BR3-00). Resistance to Abamectin in these strains was associated with significantly enhanced O-deethylation of 7-ethoxycoumarin mediated by cytochrome P450-dependent monooxygenases (MFO). The Abamectin-resistant strains NL-00 and COL-00 showed severalfold higher MFO activity than the susceptible strain GSS. Furthermore a higher glutathione S -transferase (GST) activity was detected toward 1-chloro-2,4-dinitrobenzene (CDNB) and monochlorobimane, a new substrate leading to a fluorescent product upon conjugation with glutathione. The measured 1.6- and 2.0-fold increases in GST activity toward CDNB in strains COL-00 and NL-00 were almost proportional to the resistance factors of 26 and 54, respectively. Frequency distribution of GST activity measured by the microfluorometric assay using monochlorobimane in homogenates of individual spider mites showed totally separated activity patterns for the susceptible strain GSS and the Abamectin-resistant strain NL-00. In contrast to strain NL-00, Abamectin resistance in the Brazilian strain was not stable in the laboratory over 6 months and the loss of resistance coincided with decreased GST and MFO activity. The involvement of GST and MFO in Abamectin resistance in T. urticae was confirmed by synergism studies with the MFO inhibitor piperonyl butoxide and the GST inhibitor diethyl maleate. This paper is the first attempt to biochemically describe Abamectin resistance in T. urticae .
Lin He – 2nd expert on this subject based on the ideXlab platform
functional analysis of ugt201d3 associated with Abamectin resistance in tetranychus cinnabarinus boisduvalInsect Science, 2020Co-Authors: Mengyao Wang, Guangmao Shen, Ping Zhang, Wencai Lu, Lin HeAbstract:
: Uridine diphosphate (UDP)-glycosyltransferases (UGTs) are widely distributed within living organisms and share roles in biotransformation of various lipophilic endo- and xenobiotics with activated UDP sugars. In this study, it was found that the activity of UGTs in Abamectin-resistant (AbR) strain was significantly higher (2.35-fold) than that in susceptible strain (SS) of Tetranychus cinnabarinus. Further analysis showed that 5-nitrouracil, the inhibitor of UGTs, could enhance the lethal effect of Abamectin on mites. From the previous microarray results, we found an UGT gene (UGT201D3) overexpressed in AbR strain. Quantitative PCR analysis showed that UGT201D3 was highly expressed and more inducible with Abamectin exposure in the AbR strain. After silencing the transcription of UGT201D3, the activity of UGTs was decreased and the susceptibility to Abamectin was increased in AbR strain whereas it was not in SS. Furthermore, UGT201D3 gene was then successfully expressed in Escherichia coli. The recombinant UGT201D3 exhibited α-naphthol activity (2.81 ± 0.43 nmol/mg protein/min), and the enzyme activity could be inhibited by Abamectin (inhibitory concentration at 50%: 57.50 ± 3.54 μmol/L). High-performance liquid chromatography analysis demonstrated that the recombinant UGT201D3 could effectively deplete Abamectin (15.77% ± 3.72%) incubating with 150 μg protein for 6 h. These results provided direct evidence that UGT201D3 was involved in Abamectin resistance in T. cinnabarinus.
high gama aminobutyric acid contents involved in Abamectin resistance and predation an interesting phenomenon in spider mitesFrontiers in Physiology, 2017Co-Authors: Zhifeng Xu, Wei Xiao, Guangmao Shen, Wencai Lu, Kaiyang Feng, Jinjun Wang, Guy Smagghe, Qiang Xu, Lin HeAbstract:
Abamectin has been widely used as an insecticide/acaricide for more than 30 years because of its superior bioactivity. Recently, an interesting phenomenon was identified in the carmine spider mite, Tetranychus cinnabarinus, an important pest in agriculture. The gamma aminobutyric acid (GABA) contents in a laboratory Abamectin resistant strain of T. cinnabarinus (AbR) were significantly increased. Decreases in activity and mRNA expression of GABA transaminase (GABA-T) were responsible for GABA accumulation in AbR mites. To clarify the mechanism of GABA accumulation mediated Abamectin resistance, three artificial approaches were conducted to increase GABA contents in susceptible mites, including feeding of vigabatrin (a specific inhibitor of GABA-T), feeding of exogenous GABA, and inhibition of GABA-T gene expression. The results showed that susceptible mites developed resistance to Abamectin when the GABA contents were artificially increased. We also observed that the mites with higher GABA contents moved more slowly, which is consistent with the fact that GABA is an inhibitory neurotransmitter in arthropods. Subsequently, functional response assays revealed that predation rates of predatory mites on GABA accumulated Abamectin-resistant mites were much higher than control groups. The tolerance to Abamectin, slow crawling speed, and vulnerability to predators were all resulted from GABA accumulation. This relationship between GABA and predation was also confirmed in a field-collected population. Our finding indicates that predatory mites might be used as a tool for biological control to circumvent the development of Abamectin resistance in mites.
Yidong Wu – 3rd expert on this subject based on the ideXlab platform
mutations on m3 helix of plutella xylostella glutamate gated chloride channel confer unequal resistance to Abamectin by two different mechanismsInsect Biochemistry and Molecular Biology, 2017Co-Authors: Xingliang Wang, Alin M Puinean, Andrias O O Reilly, Martin S Williamson, Charles L C Smelt, Neil S Millar, Yidong WuAbstract:
Abamectin is one of the most widely used avermectins for agricultural pests control, but the emergence of resistance around the world is proving a major threat to its sustained application. Abamectin acts by directly activating glutamate-gated chloride channels (GluCls) and modulating other Cys-loop ion channels. To date, three mutations occurring in the transmembrane domain of arthropod GluCls are associated with target-site resistance to Abamectin: A309V in Plutella xylostella GluCl (PxGluCl), G323D in Tetranychus urticae GluCl1 (TuGluCl1) and G326E in TuGluCl3. To compare the effects of these mutations in a single system, A309V/I/G and G315E (corresponding to G323 in TuGluCl1 and G326 in TuGluCl3) substitutions were introduced individually into the PxGluCl channel. Functional analysis using Xenopus oocytes showed that the A309V and G315E mutations reduced the sensitivity to Abamectin by 4.8- and 493-fold, respectively. In contrast, the substitutions A309I/G show no significant effects on the response to Abamectin. Interestingly, the A309I substitution increased the channel sensitivity to glutamate by one order of magnitude (∼12-fold). Analysis of PxGluCl homology models indicates that the G315E mutation interferes with Abamectin binding through a steric hindrance mechanism. In contrast, the structural consequences of the A309 mutations are not so clear and an allosteric modification of the binding site is the most likely mechanism. Overall the results show that both A309V and G315E mutations may contribute to target-site resistance to Abamectin and may be important for the future prediction and monitoring of Abamectin resistance in P. xylostella and other arthropod pests.
Dominant fitness costs of Abamectin resistance in Plutella xylostella.Pest Management Science, 2014Co-Authors: Ran Wang, Yidong WuAbstract:
The TH-Abm strain of Plutella xylostella, exhibiting 23 670-fold resistance to Abamectin, was selected from a field-evolved multiresistant population. By repeated backcrossing to a susceptible strain (Roth) and selection with Abamectin, the resistance trait of TH-Abm was introgressed into Roth to generate a near-isogenic strain (Roth-Abm). Fitness costs associated with Abamectin resistance were examined in Roth-Abm.
Compared with Roth, Roth-Abm obtained 11 500-fold resistance to Abamectin and 364 000-, 12- and 12-fold cross-resistance to emamectin benzoate, spinosad and fipronil respectively. Roth-Abm has a significantly longer pupal development time, lesser female pupal weight and lower larval survival than Roth. Female fecundity and egg viability are significantly lower in Roth-Abm than in Roth. All of the above fitness components of the F1 progeny from Roth × Roth-Abm are similar to those of Roth-Abm and are significantly lower than those of Roth. By comparing with the net replacement rate (R0) of Roth, the fitness of Roth-Abm, F1a (Roth male × Roth-Abm) and F1b (Roth female × Roth-Abm) are 0.50, 0.50 and 0.53 respectively.
Abamectin resistance in Roth-Abm results in significant fitness costs, and the fitness costs are autosomal and dominant. Rotation of Abamectin with other insecticides without cross-resistance could be especially useful for delaying Abamectin resistance in P. xylostella. © 2014 Society of Chemical Industry
characterisation of Abamectin resistance in a field evolved multiresistant population of plutella xylostellaPest Management Science, 2009Co-Authors: Xin Pu, Yihua Yang, Shuwen Wu, Yidong WuAbstract:
BACKGROUND:Plutella xylostella (L.) has evolved resistance to various kinds of insecticide in the field. Reversion and selection, cross-resistance, inheritance and mechanisms of Abamectin resistance were characterised in a field-derived multiresistant population of P. xylostella from China.
RESULTS: Compared with a susceptible Roth strain, the field-derived TH population showed ∼5000-fold resistance to Abamectin. Rapid reversion of Abamectin resistance was observed in the TH population when kept without insecticide selection. The TH-Abm strain, selected from the TH population with Abamectin, developed 23 670-fold resistance to Abamectin, a high level of cross-resistance to emamectin benzoate and low levels of cross-resistance to spinosad and fipronil. Genetic analyses indicated that Abamectin resistance in the TH-Abm strain was autosomal, incompletely dominant and polygenic. P450 monooxygenase activities in the TH-Abm strain were significantly elevated compared with the TH strain. Piperonyl butoxide (PBO) inhibited a small part of Abamectin resistance in the TH-Abm strain.
CONCLUSION: Field-evolved high-level resistance to Abamectin in the TH population was not stable. Selection of the TH population with Abamectin resulted in an extremely high level of cross-resistance to emamectin benzoate and low levels of cross-resistance to spinosad and fipronil. Enhanced oxidative metabolism was involved in, but may not be the major mechanism of, polygenic Abamectin resistance in the TH-Abm strain. Copyright © 2009 Society of Chemical Industry