Evidence map›Paper›PMID 28835683›Full record

ArticleScientific reports2017

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

Maria Riga, Sabina Bajda, Christos Themistokleous, Stavrini Papadaki, Maria Palzewicz, Wannes Dermauw, John Vontas, Thomas Van Leeuwen

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.3field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 102 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 4 countries.

Maria RigaDepartment of Biology, University of Crete, 70013, Heraklion, Crete, Greece.
Sabina BajdaInstitute for Biodiversity and Ecosystem Dynamics, University of Amsterdam, P.O. Box 9424, 1090 GE, Amsterdam, The Netherlands.
Christos ThemistokleousDepartment of Biology, University of Crete, 70013, Heraklion, Crete, Greece.
Stavrini PapadakiDepartment of Biology, University of Crete, 70013, Heraklion, Crete, Greece.
Maria PalzewiczInstitute for Biodiversity and Ecosystem Dynamics, University of Amsterdam, P.O. Box 9424, 1090 GE, Amsterdam, The Netherlands.
Wannes DermauwLaboratory of Agrozoology, Department of Crop Protection, Faculty of Bioscience Engineering, Coupure Links 653, Ghent University, B-9000, Ghent, Belgium.ORCID 0000-0003-4612-8969
John VontasInstitute of Molecular Biology & Biotechnology, Foundation for Research & Technology Hellas, 100 N. Plastira Street, 700 13, Heraklion, Crete, Greece.
Thomas Van LeeuwenInstitute for Biodiversity and Ecosystem Dynamics, University of Amsterdam, P.O. Box 9424, 1090 GE, Amsterdam, The Netherlands. thomas.vanleeuwen@ugent.be.
University of Crete · GRGhent University · BEUniversity of Amsterdam · NLAgricultural University of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Genetic MarkersMutationPhenotypeAcaricidesAnimalsCrosses, GeneticGenes, InsectGenes, MitochondrialInsecticide ResistanceTetranychidaeToxicity TestsAcaricidesGenetic Markers

Identifiers

PMID28835683
PMCPMC5569037
OpenAlexW2746899921

What OpenQuestion holds

Textmetadata
LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.