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

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,...

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Autores principales:	Maria Riga, Sabina Bajda, Christos Themistokleous, Stavrini Papadaki, Maria Palzewicz, Wannes Dermauw, John Vontas, Thomas Van Leeuwen
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/3554c0fff83840da8d89a4171be3f57d
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spelling	oai:doaj.org-article:3554c0fff83840da8d89a4171be3f57d2021-12-02T11:40:52ZThe relative contribution of target-site mutations in complex acaricide resistant phenotypes as assessed by marker assisted backcrossing in Tetranychus urticae10.1038/s41598-017-09054-y2045-2322https://doaj.org/article/3554c0fff83840da8d89a4171be3f57d2017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-09054-yhttps://doaj.org/toc/2045-2322Abstract 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.Maria RigaSabina BajdaChristos ThemistokleousStavrini PapadakiMaria PalzewiczWannes DermauwJohn VontasThomas Van LeeuwenNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Maria Riga Sabina Bajda Christos Themistokleous Stavrini Papadaki Maria Palzewicz Wannes Dermauw John Vontas Thomas Van Leeuwen The relative contribution of target-site mutations in complex acaricide resistant phenotypes as assessed by marker assisted backcrossing in Tetranychus urticae
description	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.
format	article
author	Maria Riga Sabina Bajda Christos Themistokleous Stavrini Papadaki Maria Palzewicz Wannes Dermauw John Vontas Thomas Van Leeuwen
author_facet	Maria Riga Sabina Bajda Christos Themistokleous Stavrini Papadaki Maria Palzewicz Wannes Dermauw John Vontas Thomas Van Leeuwen
author_sort	Maria Riga
title	The relative contribution of target-site mutations in complex acaricide resistant phenotypes as assessed by marker assisted backcrossing in Tetranychus urticae
title_short	The relative contribution of target-site mutations in complex acaricide resistant phenotypes as assessed by marker assisted backcrossing in Tetranychus urticae
title_full	The relative contribution of target-site mutations in complex acaricide resistant phenotypes as assessed by marker assisted backcrossing in Tetranychus urticae
title_fullStr	The relative contribution of target-site mutations in complex acaricide resistant phenotypes as assessed by marker assisted backcrossing in Tetranychus urticae
title_full_unstemmed	The relative contribution of target-site mutations in complex acaricide resistant phenotypes as assessed by marker assisted backcrossing in Tetranychus urticae
title_sort	relative contribution of target-site mutations in complex acaricide resistant phenotypes as assessed by marker assisted backcrossing in tetranychus urticae
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/3554c0fff83840da8d89a4171be3f57d
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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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