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

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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.
Keywords
2-SPOTTED SPIDER-MITE, GATED CHLORIDE CHANNEL, ABAMECTIN RESISTANCE, CROSS-RESISTANCE, KOCH ACARI, SODIUM-CHANNEL, DROSOPHILA-MELANOGASTER, POINT MUTATION, INSECTICIDE RESISTANCE, HEXYTHIAZOX RESISTANCE

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Chicago
Riga, Maria, Sabina Bajda, Christos Themistokleous, Stavrini Papadaki, Maria Palzewicz, Wannes Dermauw, John Vontas, and Thomas Van Leeuwen. 2017. “The Relative Contribution of Target-site Mutations in Complex Acaricide Resistant Phenotypes as Assessed by Marker Assisted Backcrossing in Tetranychus Urticae.” Scientific Reports 7.
APA
Riga, Maria, Bajda, S., Themistokleous, C., Papadaki, S., Palzewicz, M., Dermauw, W., Vontas, J., et al. (2017). The relative contribution of target-site mutations in complex acaricide resistant phenotypes as assessed by marker assisted backcrossing in Tetranychus urticae. SCIENTIFIC REPORTS, 7.
Vancouver
1.
Riga M, Bajda S, Themistokleous C, Papadaki S, Palzewicz M, Dermauw W, et al. The relative contribution of target-site mutations in complex acaricide resistant phenotypes as assessed by marker assisted backcrossing in Tetranychus urticae. SCIENTIFIC REPORTS. 2017;7.
MLA
Riga, Maria, Sabina Bajda, Christos Themistokleous, et al. “The Relative Contribution of Target-site Mutations in Complex Acaricide Resistant Phenotypes as Assessed by Marker Assisted Backcrossing in Tetranychus Urticae.” SCIENTIFIC REPORTS 7 (2017): n. pag. Print.
@article{8538955,
  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.},
  articleno    = {9202},
  author       = {Riga, Maria and Bajda, Sabina and Themistokleous, Christos and Papadaki, Stavrini and Palzewicz, Maria and Dermauw, Wannes and Vontas, John and Van Leeuwen, Thomas},
  issn         = {2045-2322},
  journal      = {SCIENTIFIC REPORTS},
  keyword      = {2-SPOTTED SPIDER-MITE,GATED CHLORIDE CHANNEL,ABAMECTIN RESISTANCE,CROSS-RESISTANCE,KOCH ACARI,SODIUM-CHANNEL,DROSOPHILA-MELANOGASTER,POINT MUTATION,INSECTICIDE RESISTANCE,HEXYTHIAZOX RESISTANCE},
  language     = {eng},
  pages        = {12},
  title        = {The relative contribution of target-site mutations in complex acaricide resistant phenotypes as assessed by marker assisted backcrossing in Tetranychus urticae},
  url          = {http://dx.doi.org/10.1038/s41598-017-09054-y},
  volume       = {7},
  year         = {2017},
}

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