Evidence map›Paper›PMID 32430396›Full record

ReviewThe Journal of biological chemistry2020

Mechanisms of evolved herbicide resistance.

Todd A Gaines, Stephen O Duke, Sarah Morran, Carlos A G Rigon, Patrick J Tranel, Anita Küpper, Franck E Dayan

Open access · hybridAbstract readReview
In one paragraph

Review in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 188 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
188citing papers in PubMed, 1 pooled it
75.8field-weighted citation impact, top 1% 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

188 citing papers in PubMed, 1 synthesis or guideline pooled it, 627 citations in OpenAlex.

  1. Pooled it
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  12. Genome-Wide Characterization of thePlants (Basel, Switzerland) · 2026
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128 more citing papers are in PubMed but not listed here.

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

7 authors at 4 institutions in 2 countries.

Todd A GainesAgricultural Biology Department, Colorado State University, Fort Collins, Colorado, USA.ORCID 0000-0003-1485-7665
Stephen O DukeNational Center for Natural Products Research, School of Pharmacy, University of Mississippi, Oxford, Mississippi, USA sduke@olemiss.edu.ORCID 0000-0001-7210-5168
Sarah MorranAgricultural Biology Department, Colorado State University, Fort Collins, Colorado, USA.
Carlos A G RigonAgricultural Biology Department, Colorado State University, Fort Collins, Colorado, USA.ORCID 0000-0001-8565-7383
Patrick J TranelDepartment of Crop Sciences, University of Illinois, Urbana, Illinois, USA.ORCID 0000-0003-0666-4564
Anita KüpperBayer AG, CropScience Division, Frankfurt am Main, Germany.ORCID 0000-0001-5122-1514
Franck E DayanAgricultural Biology Department, Colorado State University, Fort Collins, Colorado, USA.ORCID 0000-0001-6964-2499
Colorado State University · USBayer (Germany) · DEUniversity of Illinois Urbana-Champaign · USUniversity of Mississippi · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The widely successful use of synthetic herbicides over the past 70 years has imposed strong and widespread selection pressure, leading to the evolution of herbicide resistance in hundreds of weed species. Both target-site resistance (TSR) and nontarget-site resistance (NTSR) mechanisms have evolved to most herbicide classes. TSR often involves mutations in genes encoding the protein targets of herbicides, affecting the binding of the herbicide either at or near catalytic domains or in regions affecting access to them. Most of these mutations are nonsynonymous SNPs, but polymorphisms in more than one codon or entire codon deletions have also evolved. Some herbicides bind multiple proteins, making the evolution of TSR mechanisms more difficult. Increased amounts of protein target, by increased gene expression or by gene duplication, are an important, albeit less common, TSR mechanism. NTSR mechanisms include reduced absorption or translocation and increased sequestration or metabolic degradation. The mechanisms that can contribute to NTSR are complex and often involve genes that are members of large gene families. For example, enzymes involved in herbicide metabolism-based resistances include cytochromes P450, GSH

Indexed as

AcclimatizationCytochrome P-450 Enzyme SystemGene Expression Regulation, EnzymologicGene Expression Regulation, PlantHerbicide ResistanceHerbicidesPlant ProteinsPlantsCytochrome P-450 Enzyme SystemHerbicidesPlant Proteinscross-resistanceCytochrome P450evolutionglutathione S-transferaseherbicideherbicide metabolismmultiple resistancemutantnontarget-site resistanceplant biochemistryplant defenseplant evolutionplant molecular biologyplant physiologyreduced translocationresistance mechanismselection pressuretarget-site resistancexenobiotic

Identifiers

PMID32430396
PMCPMC7383398
OpenAlexW3026615616

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.