The potential of VKORC1 polymorphisms in Mustelidae for evolving anticoagulant resistance through selection along the food chain

In response to strong selection, new mutations can arise quickly and sweep through populations, particularly, if survival and reproduction depend on certain allele copies for adaptation to rapidly changing environments, like resistance against deadly diseases or strong toxins. Since the 1950s, resis...

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Veröffentlicht in:PloS one 2019-08, Vol.14 (8), p.e0221706
Hauptverfasser: Stöck, Matthias, Reisch, Florian, Elmeros, Morten, Gabriel, Doreen, Kloas, Werner, Kreuz, Eva, Lassen, Pia, Esther, Alexandra
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container_issue 8
container_start_page e0221706
container_title PloS one
container_volume 14
creator Stöck, Matthias
Reisch, Florian
Elmeros, Morten
Gabriel, Doreen
Kloas, Werner
Kreuz, Eva
Lassen, Pia
Esther, Alexandra
description In response to strong selection, new mutations can arise quickly and sweep through populations, particularly, if survival and reproduction depend on certain allele copies for adaptation to rapidly changing environments, like resistance against deadly diseases or strong toxins. Since the 1950s, resistance to anticoagulant rodenticides in several rodents has emerged through single nucleotide mutations in the vitamin-K-epoxid-reductase-complex-subunit-1 (VKORC1) gene, often located in its exon 3. Detection of high prevalence and concentrations of anticoagulant rodenticides in non-target vertebrates, including carnivorous Mustelidae, let us assume that secondary exposure by feeding on poisoned prey may also cause selection along the food chain and we hypothesized that VKORC1-based resistance might also have evolved in rodents' predators. Using newly-developed mustelid-specific primers for direct sequencing of genomic DNA, we studied VKORC1-DNA-polymorphisms in 115 mustelids of five species (Martes martes, M. foina, Mustela nivalis, M. erminea, M. putorius), obtained from northern Denmark, yielding six sites with nonsynonymous and several synonymous amino acid polymorphisms in exon 3. Comparison of these VKORC1-genotypes with hepatic rodenticide residues (obtained by HPLC combined with fluorescence or mass spectrometry) in 83 individuals (except M. martes), using generalized linear models, suggested that anticoagulant levels depended on species and specific polymorphisms. Although most VKORC-1 polymorphisms may present standing genetic variation, some are situated in resistance-mediating membrane parts of the VKORC1-encoded protein, and might be a result of selection due to exposure to anticoagulant poisons. Our new molecular markers might allow detecting indirect effects of anticoagulant rodenticides on rodent predator populations in the future.
doi_str_mv 10.1371/journal.pone.0221706
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Comparison of these VKORC1-genotypes with hepatic rodenticide residues (obtained by HPLC combined with fluorescence or mass spectrometry) in 83 individuals (except M. martes), using generalized linear models, suggested that anticoagulant levels depended on species and specific polymorphisms. Although most VKORC-1 polymorphisms may present standing genetic variation, some are situated in resistance-mediating membrane parts of the VKORC1-encoded protein, and might be a result of selection due to exposure to anticoagulant poisons. 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Since the 1950s, resistance to anticoagulant rodenticides in several rodents has emerged through single nucleotide mutations in the vitamin-K-epoxid-reductase-complex-subunit-1 (VKORC1) gene, often located in its exon 3. Detection of high prevalence and concentrations of anticoagulant rodenticides in non-target vertebrates, including carnivorous Mustelidae, let us assume that secondary exposure by feeding on poisoned prey may also cause selection along the food chain and we hypothesized that VKORC1-based resistance might also have evolved in rodents' predators. Using newly-developed mustelid-specific primers for direct sequencing of genomic DNA, we studied VKORC1-DNA-polymorphisms in 115 mustelids of five species (Martes martes, M. foina, Mustela nivalis, M. erminea, M. putorius), obtained from northern Denmark, yielding six sites with nonsynonymous and several synonymous amino acid polymorphisms in exon 3. 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1932-6203
language eng
recordid cdi_plos_journals_2282685080
source MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry
subjects Adaptation
Amino acids
Amino Acids - genetics
Animals
Anticoagulants
Anticoagulants - pharmacology
Aquaculture
Binding sites
Biology and Life Sciences
Changing environments
Denmark
Deoxyribonucleic acid
DNA
DNA sequencing
Ecology and Environmental Sciences
Environmental changes
Exons - genetics
Exposure
Fisheries
Fluorescence
Food Chain
Food chains
Food selection
Freshwater ecology
Gene sequencing
Genes
Genetic aspects
Genetic diversity
Genetic polymorphisms
Genetic research
Genotypes
Geography
High performance liquid chromatography
Insecticide resistance
Introns - genetics
Liquid chromatography
Martes martes
Mass spectrometry
Mass spectroscopy
Mustelidae
Mustelidae - genetics
Mutation
Nucleotides
Physical sciences
Poisons
Polymorphism, Genetic
Population genetics
Populations
Predators
Prey
Primers
Proteins
Reductase
Reductases
Research and Analysis Methods
Rodenticides
Rodents
Soil sciences
Spectroscopy
Statistical models
Systematic review
Toxins
Vertebrates
Vitamin K Epoxide Reductases - genetics
Vitamins
title The potential of VKORC1 polymorphisms in Mustelidae for evolving anticoagulant resistance through selection along the food chain
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