The relative contribution of target-site mutations in complex acaricide resistant phenotypes as assessed by marker assisted backcrossing in Tetranychus urticae

The mechanisms underlying insecticide and acaricide resistance in insects and mites are often complex, including additive effects of target-site insensitivity, increased metabolism and transport. The extent to which target-site resistance mutations contribute to the resistance phenotype is, however,...

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Published inScientific reports Vol. 7; no. 1; pp. 9202 - 12
Main Authors Riga, Maria, Bajda, Sabina, Themistokleous, Christos, Papadaki, Stavrini, Palzewicz, Maria, Dermauw, Wannes, Vontas, John, Leeuwen, Thomas Van
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 23.08.2017
Nature Publishing Group
Nature Portfolio
Subjects
45
45/22
45/23
45/77
631/1647/1513/2216
631/181/2474
631/208/8
Abamectin
Acaricides
Chitin
Chitin synthase
Chloride channels
Chlorides
Cytochrome b
Fungicides
Humanities and Social Sciences
Insecticides
Mites
Mitochondria
multidisciplinary
Mutation
Pyrethroids
Science
Science (multidisciplinary)
Sodium channels (voltage-gated)
Tetranychus urticae
Toxicity
Online AccessGet full text
ISSN2045-2322
2045-2322
DOI10.1038/s41598-017-09054-y

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Abstract The mechanisms underlying insecticide and acaricide resistance in insects and mites are often complex, including additive effects of target-site insensitivity, increased metabolism and transport. The extent to which target-site resistance mutations contribute to the resistance phenotype is, however, not well studied. Here, we used marker-assisted backcrossing to create 30 congenic lines carrying nine mutations (alone, or in combination in a few cases) associated with resistance to avermectins, pyrethroids, mite growth inhibitors and mitochondrial complex III inhibitors (QoI) in a polyphagous arthropod pest, the spider mite Tetranychus urticae . Toxicity tests revealed that mutations in the voltage-gated sodium channel, chitin synthase 1 and cytochrome b confer high levels of resistance and, when fixed in a population, these mutations alone can result in field failure of acaricide treatment. In contrast, although we confirmed the implication of mutations in glutamate-gated chloride channels in abamectin and milbemectin insensitivity, these mutations do not lead to the high resistance levels that are often reported in abamectin resistant strains of T. urticae . Overall, this study functionally validates reported target-site resistance mutations in T. urticae , by uncoupling them from additional mechanisms, allowing to finally investigate the strength of the conferred phenotype in vivo .
AbstractList The mechanisms underlying insecticide and acaricide resistance in insects and mites are often complex, including additive effects of target-site insensitivity, increased metabolism and transport. The extent to which target-site resistance mutations contribute to the resistance phenotype is, however, not well studied. Here, we used marker-assisted backcrossing to create 30 congenic lines carrying nine mutations (alone, or in combination in a few cases) associated with resistance to avermectins, pyrethroids, mite growth inhibitors and mitochondrial complex III inhibitors (QoI) in a polyphagous arthropod pest, the spider mite Tetranychus urticae . Toxicity tests revealed that mutations in the voltage-gated sodium channel, chitin synthase 1 and cytochrome b confer high levels of resistance and, when fixed in a population, these mutations alone can result in field failure of acaricide treatment. In contrast, although we confirmed the implication of mutations in glutamate-gated chloride channels in abamectin and milbemectin insensitivity, these mutations do not lead to the high resistance levels that are often reported in abamectin resistant strains of T. urticae . Overall, this study functionally validates reported target-site resistance mutations in T. urticae , by uncoupling them from additional mechanisms, allowing to finally investigate the strength of the conferred phenotype in vivo .
The mechanisms underlying insecticide and acaricide resistance in insects and mites are often complex, including additive effects of target-site insensitivity, increased metabolism and transport. The extent to which target-site resistance mutations contribute to the resistance phenotype is, however, not well studied. Here, we used marker-assisted backcrossing to create 30 congenic lines carrying nine mutations (alone, or in combination in a few cases) associated with resistance to avermectins, pyrethroids, mite growth inhibitors and mitochondrial complex III inhibitors (QoI) in a polyphagous arthropod pest, the spider mite Tetranychus urticae. Toxicity tests revealed that mutations in the voltage-gated sodium channel, chitin synthase 1 and cytochrome b confer high levels of resistance and, when fixed in a population, these mutations alone can result in field failure of acaricide treatment. In contrast, although we confirmed the implication of mutations in glutamate-gated chloride channels in abamectin and milbemectin insensitivity, these mutations do not lead to the high resistance levels that are often reported in abamectin resistant strains of T. urticae. Overall, this study functionally validates reported target-site resistance mutations in T. urticae, by uncoupling them from additional mechanisms, allowing to finally investigate the strength of the conferred phenotype in vivo.
Abstract The mechanisms underlying insecticide and acaricide resistance in insects and mites are often complex, including additive effects of target-site insensitivity, increased metabolism and transport. The extent to which target-site resistance mutations contribute to the resistance phenotype is, however, not well studied. Here, we used marker-assisted backcrossing to create 30 congenic lines carrying nine mutations (alone, or in combination in a few cases) associated with resistance to avermectins, pyrethroids, mite growth inhibitors and mitochondrial complex III inhibitors (QoI) in a polyphagous arthropod pest, the spider mite Tetranychus urticae. Toxicity tests revealed that mutations in the voltage-gated sodium channel, chitin synthase 1 and cytochrome b confer high levels of resistance and, when fixed in a population, these mutations alone can result in field failure of acaricide treatment. In contrast, although we confirmed the implication of mutations in glutamate-gated chloride channels in abamectin and milbemectin insensitivity, these mutations do not lead to the high resistance levels that are often reported in abamectin resistant strains of T. urticae. Overall, this study functionally validates reported target-site resistance mutations in T. urticae, by uncoupling them from additional mechanisms, allowing to finally investigate the strength of the conferred phenotype in vivo.
The mechanisms underlying insecticide and acaricide resistance in insects and mites are often complex, including additive effects of target-site insensitivity, increased metabolism and transport. The extent to which target-site resistance mutations contribute to the resistance phenotype is, however, not well studied. Here, we used marker-assisted backcrossing to create 30 congenic lines carrying nine mutations (alone, or in combination in a few cases) associated with resistance to avermectins, pyrethroids, mite growth inhibitors and mitochondrial complex III inhibitors (QoI) in a polyphagous arthropod pest, the spider mite Tetranychus urticae. Toxicity tests revealed that mutations in the voltage-gated sodium channel, chitin synthase 1 and cytochrome b confer high levels of resistance and, when fixed in a population, these mutations alone can result in field failure of acaricide treatment. In contrast, although we confirmed the implication of mutations in glutamate-gated chloride channels in abamectin and milbemectin insensitivity, these mutations do not lead to the high resistance levels that are often reported in abamectin resistant strains of T. urticae. Overall, this study functionally validates reported target-site resistance mutations in T. urticae, by uncoupling them from additional mechanisms, allowing to finally investigate the strength of the conferred phenotype in vivo.The mechanisms underlying insecticide and acaricide resistance in insects and mites are often complex, including additive effects of target-site insensitivity, increased metabolism and transport. The extent to which target-site resistance mutations contribute to the resistance phenotype is, however, not well studied. Here, we used marker-assisted backcrossing to create 30 congenic lines carrying nine mutations (alone, or in combination in a few cases) associated with resistance to avermectins, pyrethroids, mite growth inhibitors and mitochondrial complex III inhibitors (QoI) in a polyphagous arthropod pest, the spider mite Tetranychus urticae. Toxicity tests revealed that mutations in the voltage-gated sodium channel, chitin synthase 1 and cytochrome b confer high levels of resistance and, when fixed in a population, these mutations alone can result in field failure of acaricide treatment. In contrast, although we confirmed the implication of mutations in glutamate-gated chloride channels in abamectin and milbemectin insensitivity, these mutations do not lead to the high resistance levels that are often reported in abamectin resistant strains of T. urticae. Overall, this study functionally validates reported target-site resistance mutations in T. urticae, by uncoupling them from additional mechanisms, allowing to finally investigate the strength of the conferred phenotype in vivo.
ArticleNumber 9202
Author Papadaki, Stavrini
Riga, Maria
Vontas, John
Leeuwen, Thomas Van
Themistokleous, Christos
Dermauw, Wannes
Bajda, Sabina
Palzewicz, Maria
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  fullname: Leeuwen, Thomas Van
  email: thomas.vanleeuwen@ugent.be
  organization: Institute for Biodiversity and Ecosystem Dynamics, University of Amsterdam, P.O. Box 9424, Laboratory of Agrozoology, Department of Crop Protection, Faculty of Bioscience Engineering, Coupure Links 653, Ghent University
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– volume: 67
  start-page: 1285
  year: 2011
  ident: 9054_CR30
  publication-title: Pest Manag Sci
  doi: 10.1002/ps.2184
– volume: 72
  start-page: 111
  year: 2002
  ident: 9054_CR74
  publication-title: Pestic Biochem Phys
  doi: 10.1006/pest.2001.2583
– ident: 9054_CR81
SSID ssj0000529419
Score 2.478397
Snippet The mechanisms underlying insecticide and acaricide resistance in insects and mites are often complex, including additive effects of target-site insensitivity,...
Abstract The mechanisms underlying insecticide and acaricide resistance in insects and mites are often complex, including additive effects of target-site...
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SubjectTerms 45
45/22
45/23
45/77
631/1647/1513/2216
631/181/2474
631/208/8
Abamectin
Acaricides
Chitin
Chitin synthase
Chloride channels
Chlorides
Cytochrome b
Fungicides
Humanities and Social Sciences
Insecticides
Mites
Mitochondria
multidisciplinary
Mutation
Pyrethroids
Science
Science (multidisciplinary)
Sodium channels (voltage-gated)
Tetranychus urticae
Toxicity
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Title The relative contribution of target-site mutations in complex acaricide resistant phenotypes as assessed by marker assisted backcrossing in Tetranychus urticae
URI https://link.springer.com/article/10.1038/s41598-017-09054-y
https://www.ncbi.nlm.nih.gov/pubmed/28835683
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https://www.proquest.com/docview/1932168854
https://pubmed.ncbi.nlm.nih.gov/PMC5569037
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