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Luc Tirry - One of the best experts on this subject based on the ideXlab platform.
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mutations in the mitochondrial cytochrome b of tetranychus urticae koch acari tetranychidae confer Cross Resistance between bifenazate and acequinocyl
Pest Management Science, 2009Co-Authors: Pieter Van Nieuwenhuyse, Thomas Van Leeuwen, Jahangir Khajehali, Bartel Vanholme, Luc TirryAbstract:BACKGROUND: Resistance of Tetranychus urticae Koch to bifenazate was recently linked with mutations in the mitochondrial cytochrome b Qo pocket, suggesting that bifenazate acts as a Qo inhibitor (QoI). Since these mutations might cause Cross-Resistance to the known acaricidal QoI acequinocyl and fluacrypyrim, Resistance levels and inheritance patterns were investigated in several bifenazate-susceptible and bifenazate-resistant strains with different mutations in the cd1 and ef helices aligning the Qo pocket. RESULTS: Cross-Resistance to acequinocyl in two bifenazate-resistant strains was shown to be maternally inherited and caused by the combination of two specific mutations in the cytochrome b Qo pocket. Although most investigated strains were resistant to fluacrypyrim, Resistance was not inherited maternally, but as a monogenic autosomal highly dominant trait. As a consequence, there was no correlation between cytochrome b genotype and fluacrypyrim Resistance. CONCLUSIONS: Although there is no absolute Cross-Resistance between bifenazate, acequinocyl and fluacrypyrim, some bifenazate Resistance mutations confer Cross-Resistance to acequinocyl. In the light of Resistance development and management, high prudence is called for when alternating bifenazate and acequinocyl in the same crop. Maternally inherited Cross-Resistance between bifenazate and acequinocyl reinforces the likelihood of bifenazate acting as a mitochondrial complex III inhibitor at the Qo site. Copyright © 2009 Society of Chemical Industry
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mutations in the mitochondrial cytochrome b of tetranychus urticae koch acari tetranychidae confer Cross Resistance between bifenazate and acequinocyl
Pest Management Science, 2009Co-Authors: Pieter Van Nieuwenhuyse, Jahangir Khajehali, Bartel Vanholme, Thomas Van Leeuwen, Luc TirryAbstract:BACKGROUND: Resistance of Tetranychus urticae Koch to bifenazate was recently linked with mutations in the mitochondrial cytochrome b Qo pocket, suggesting that bifenazate acts as a Qo inhibitor (QoI). Since these mutations might cause Cross-Resistance to the known acaricidal QoI acequinocyl and fluacrypyrim, Resistance levels and inheritance patterns were investigated in several bifenazate-susceptible and bifenazate-resistant strains with different mutations in the cd1 and ef helices aligning the Qo pocket. RESULTS: Cross-Resistance to acequinocyl in two bifenazate-resistant strains was shown to be maternally inherited and caused by the combination of two specific mutations in the cytochrome b Qo pocket. Although most investigated strains were resistant to fluacrypyrim, Resistance was not inherited maternally, but as a monogenic autosomal highly dominant trait. As a consequence, there was no correlation between cytochrome b genotype and fluacrypyrim Resistance. CONCLUSIONS: Although there is no absolute Cross-Resistance between bifenazate, acequinocyl and fluacrypyrim, some bifenazate Resistance mutations confer Cross-Resistance to acequinocyl. In the light of Resistance development and management, high prudence is called for when alternating bifenazate and acequinocyl in the same crop. Maternally inherited Cross-Resistance between bifenazate and acequinocyl reinforces the likelihood of bifenazate acting as a mitochondrial complex III inhibitor at the Qo site. Copyright © 2009 Society of Chemical Industry
Xiwu Gao - One of the best experts on this subject based on the ideXlab platform.
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Cross Resistance patterns and fitness in fufenozide resistant diamondback moth plutella xylostella lepidoptera plutellidae
Pest Management Science, 2012Co-Authors: Jingyan Sun, Pei Liang, Xiwu GaoAbstract:BACKGROUND: Fufenozide is a novel non-steroidal ecdysone agonist with good efficacy against diamondback moth (DBM), Plutella xylostella (Lepidoptera: Plutellidae). At present, it is widely applied for the control of a range of lepidopterous pests in China. This study compared the activities of fufenozide and 12 other insecticides against unselected and fufenozide-selected strains of DBM to examine potential patterns of Cross-Resistance. The relative fitness of the fufenozide-selected strain was assessed to provide information pertinent to insecticide Resistance management. RESULTS: Compared with the susceptible strain (JSS), the fufenozide-resistant strain (JSR) showed high Cross-Resistance to dibenzoylhydrazines and benzoylphenylureas, low Cross-Resistance to abamectin and no Cross-Resistance to organophosphates, carbamates and pyrethroids. JSR had a lower reproductive ability and a relative fitness of 0.5 compared with JSS. CONCLUSION:P. xylostella has the potential to develop Resistance to fufenozide, albeit at the expense of fitness. Cross-Resistance between the same and other classes of insecticides is of concern, and should be a key consideration when implementing fufenozide-based control strategies for this species. Copyright © 2011 Society of Chemical Industry
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genetic basis of Resistance and studies on Cross Resistance in a population of diamondback moth plutella xylostella lepidoptera plutellidae
Pest Management Science, 2003Co-Authors: Pei Liang, Xiwu Gao, Bingzong ZhengAbstract:The genetic basis of abamectin Resistance was studied in a strain of the diamondback moth, Plutella xylostella (L), following laboratory selection of a field population collected at Xuanhua, Hebei Province, China. Data from the testing of F1 progeny from reciprocal Crosses between abamectin-resistant and abamectin-susceptible strains indicated that Resistance might be autosomal and incompletely recessive with a degree of dominance of -0.13. Chi-squared analyses from the response of a backCross of Crossed F1 progeny and the resistant strain and F2 progeny were highly significant, suggesting that the Resistance was probably controlled by more than one gene. The results of Cross-Resistance studies showed that there was little Cross-Resistance between abamectin and four pyrethroid insecticides (deltamethrin, beta-cypermethrin, fenvalerate and bifenthrin) and no Cross-Resistance between abamectin and the acylureas chlorfluazuron or flufenoxuron.
Youjun Zhang - One of the best experts on this subject based on the ideXlab platform.
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Cross Resistance and biochemical mechanisms of abamectin Resistance in the western flower thrips frankliniella occidentalis
Pesticide Biochemistry and Physiology, 2011Co-Authors: Xuelin Chen, Linze Yuan, Yuzhou Du, Youjun Zhang, Jianjun WangAbstract:Abamectin Resistance was selected in the western flower thrips [Frankliniella occidentalis (Pergande)] under the laboratory conditions, and Cross-Resistance patterns and possible Resistance mechanisms in the abamectin-resistant strain (ABA-R) were investigated. Compared with the susceptible strain (ABA-S), the ABA-R strain displayed 45.5-fold Resistance to abamectin after 15 selection cycles during 18 generations. Rapid reversion of abamectin Resistance was observed in the ABA-R strain in the absence of the insecticide selection pressure. Moderate and low levels of Cross-Resistance to chlorpyrifos (RR 11.4) and lambda-cyhalothrin (3.98) were observed in the ABA-R strain, but no significant Cross-Resistance was found to spinosad (2.00), acetamiprid (1.47) and chlorfenapyr (0.26). Our studies also showed that the esterase inhibitor S,S,S-tributyl phosphorotrithioate (DEF) and glutathione S-transferase inhibitor diethyl maleate (DEM) were not able to synergize the toxicity of abamectin, whereas the oxidase inhibitor piperonyl butoxide (PBO) conferred a significant synergism on abamectin in the ABA-R strain (SR 3.00). Biochemical analysis showed that cytochrome P450 monooxygenase activity of the ABA-R strain was 6.66-fold higher than that of the ABA-S strain. It appears that enhanced oxidative metabolism mediated by cytochrome P450 monooxygenases was a major mechanism for abamectin Resistance in the western flower thrips.
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Cross Resistance study and biochemical mechanisms of thiamethoxam Resistance in b biotype bemisia tabaci hemiptera aleyrodidae
Pest Management Science, 2010Co-Authors: Yuntao Feng, Qingjun Wu, Shaoli Wang, Xiaoli Chang, Baoyun Xu, Youjun ZhangAbstract:BACKGROUND: B-biotype Bemisia tabaci (Gennadius) has invaded China over the past two decades. To understand the risks and to determine possible mechanisms of Resistance to thiamethoxam in B. tabaci, a resistant strain was selected in the laboratory. Cross-Resistance and the biochemical mechanisms of thiamethoxam Resistance were investigated in the present study. RESULTS: A 66.3-fold thiamethoxam-resistant B. tabaci strain (TH-R) was established after selection for 36 generations. Compared with the susceptible strain (TH-S), the selected TH-R strain showed obvious Cross-Resistance to imidacloprid (47.3-fold), acetamiprid (35.8-fold), nitenpyram (9.99-fold), abamectin (5.33-fold) and carbosulfan (4.43-fold). No Cross-Resistance to fipronil, chlorpyrifos or deltamethrin was seen. Piperonyl butoxide (PBO) and triphenyl phosphate (TPP) exhibited significant synergism on thiamethoxam effects in the TH-R strain (3.14- and 2.37-fold respectively). However, diethyl maleate (DEM) did not act synergistically with thiamethoxam. Biochemical assays showed that cytochrome P450 monooxygenase activities increased 1.21- and 1.68-fold respectively, and carboxylesterase activity increased 2.96-fold in the TH-R strain. However, no difference was observed for glutathione S-transferase between the two strains. CONCLUSION: B-biotype B. tabaci develops Resistance to thiamethoxam. Cytochrome P450 monooxygenase and carboxylesterase appear to be responsible for the Resistance. Reasonable Resistance management that avoids the use of Cross-Resistance insecticides may delay the development of Resistance to thiamethoxam in this species.
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Cross Resistance study and biochemical mechanisms of thiamethoxam Resistance in b biotype bemisia tabaci hemiptera aleyrodidae
Pest Management Science, 2010Co-Authors: Yuntao Feng, Shaoli Wang, Xiaoli Chang, Wen Xie, Youjun ZhangAbstract:BACKGROUND: B-biotype Bemisia tabaci (Gennadius) has invaded China over the past two decades. To understand the risks and to determine possible mechanisms of Resistance to thiamethoxam in B. tabaci, a resistant strain was selected in the laboratory. Cross-Resistance and the biochemical mechanisms of thiamethoxam Resistance were investigated in the present study. RESULTS: A 66.3-fold thiamethoxam-resistant B. tabaci strain (TH-R) was established after selection for 36 generations. Compared with the susceptible strain (TH-S), the selected TH-R strain showed obvious Cross-Resistance to imidacloprid (47.3-fold), acetamiprid (35.8-fold), nitenpyram (9.99-fold), abamectin (5.33-fold) and carbosulfan (4.43-fold). No Cross-Resistance to fipronil, chlorpyrifos or deltamethrin was seen. Piperonyl butoxide (PBO) and triphenyl phosphate (TPP) exhibited significant synergism on thiamethoxam effects in the TH-R strain (3.14- and 2.37-fold respectively). However, diethyl maleate (DEM) did not act synergistically with thiamethoxam. Biochemical assays showed that cytochrome P450 monooxygenase activities increased 1.21- and 1.68-fold respectively, and carboxylesterase activity increased 2.96-fold in the TH-R strain. However, no difference was observed for glutathione S-transferase between the two strains. CONCLUSION: B-biotype B. tabaci develops Resistance to thiamethoxam. Cytochrome P450 monooxygenase and carboxylesterase appear to be responsible for the Resistance. Reasonable Resistance management that avoids the use of Cross-Resistance insecticides may delay the development of Resistance to thiamethoxam in this species. Copyright © 2009 Society of Chemical Industry
K D Ninsin - One of the best experts on this subject based on the ideXlab platform.
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Cross Resistance assessment in cartap and esfenvalerateselected strains of the diamondback moth plutella xylostella l lepidoptera plutellidae
West African Journal of Applied Ecology, 2015Co-Authors: K D NinsinAbstract:Effective control of the diamondback moth (DBM), Plutella xylostella (L.) (Lepidoptera: Plutellidae) has become critical due to the genetic ability of the insect pest to develop Resistance to insecticides. Alternating or rotating the use of insecticides that do not show Cross-Resistance is an important component of an effective Resistance management strategy, as it helps prevent Resistance development or regain susceptibility in an already resistant arthropod pest population. In this study, Cross-Resistance to selected insecticides in cartap- and esfenvalerate-selected strains of DBM was assessed in the laboratory, using the leaf-dipping method. The esfenvalerate-selected strain exhibited moderate Cross-Resistance to abamectin and a very low Cross-Resistance to cartap. The cartap-selected strain also displayed a very low Cross-Resistance to esfenvalerate but showed no Cross-Resistance to abamectin. Alternating cartap and abamectin would therefore help to effectively manage insecticide-Resistance development in the DBM.
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acetamiprid Resistance and Cross Resistance in the diamondback moth plutella xylostella
Pest Management Science, 2004Co-Authors: K D NinsinAbstract:A 110-fold acetamiprid-resistant Plutella xylostella (L) strain was established after four selection experiments (in five generations) on a 9.5-fold resistant colony in the laboratory. The resistant strain did not show Cross-Resistance to chlorfluazuron or Bacillus thuringiensis subsp kurstaki Berliner, but displayed low Resistance to cartap and phenthoate.
Pei Liang - One of the best experts on this subject based on the ideXlab platform.
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Cross Resistance patterns and fitness in fufenozide resistant diamondback moth plutella xylostella lepidoptera plutellidae
Pest Management Science, 2012Co-Authors: Jingyan Sun, Pei Liang, Xiwu GaoAbstract:BACKGROUND: Fufenozide is a novel non-steroidal ecdysone agonist with good efficacy against diamondback moth (DBM), Plutella xylostella (Lepidoptera: Plutellidae). At present, it is widely applied for the control of a range of lepidopterous pests in China. This study compared the activities of fufenozide and 12 other insecticides against unselected and fufenozide-selected strains of DBM to examine potential patterns of Cross-Resistance. The relative fitness of the fufenozide-selected strain was assessed to provide information pertinent to insecticide Resistance management. RESULTS: Compared with the susceptible strain (JSS), the fufenozide-resistant strain (JSR) showed high Cross-Resistance to dibenzoylhydrazines and benzoylphenylureas, low Cross-Resistance to abamectin and no Cross-Resistance to organophosphates, carbamates and pyrethroids. JSR had a lower reproductive ability and a relative fitness of 0.5 compared with JSS. CONCLUSION:P. xylostella has the potential to develop Resistance to fufenozide, albeit at the expense of fitness. Cross-Resistance between the same and other classes of insecticides is of concern, and should be a key consideration when implementing fufenozide-based control strategies for this species. Copyright © 2011 Society of Chemical Industry
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genetic basis of Resistance and studies on Cross Resistance in a population of diamondback moth plutella xylostella lepidoptera plutellidae
Pest Management Science, 2003Co-Authors: Pei Liang, Xiwu Gao, Bingzong ZhengAbstract:The genetic basis of abamectin Resistance was studied in a strain of the diamondback moth, Plutella xylostella (L), following laboratory selection of a field population collected at Xuanhua, Hebei Province, China. Data from the testing of F1 progeny from reciprocal Crosses between abamectin-resistant and abamectin-susceptible strains indicated that Resistance might be autosomal and incompletely recessive with a degree of dominance of -0.13. Chi-squared analyses from the response of a backCross of Crossed F1 progeny and the resistant strain and F2 progeny were highly significant, suggesting that the Resistance was probably controlled by more than one gene. The results of Cross-Resistance studies showed that there was little Cross-Resistance between abamectin and four pyrethroid insecticides (deltamethrin, beta-cypermethrin, fenvalerate and bifenthrin) and no Cross-Resistance between abamectin and the acylureas chlorfluazuron or flufenoxuron.