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

• Published in: Scientific 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
• Language: English
• 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
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-017-09054-y

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 .