Evidence map›Paper›PMID 29971903›Full record

ArticleBiological reviews of the Cambridge Philosophical Society2019

The evolutionary origins of pesticide resistance.

Nichola J Hawkins, Chris Bass, Andrea Dixon, Paul Neve

Open access · hybridAbstract read
In one paragraph

Article in Biological reviews of the Cambridge Philosophical Society, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 234 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
234citing papers in PubMed, 2 pooled it
74.7field-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

234 citing papers in PubMed, 2 syntheses or guidelines pooled it, 796 citations in OpenAlex.

  1. Pooled it
  2. The Use ofCannabis and cannabinoid research · 2022
    Pooled it
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174 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

4 authors at 3 institutions in 2 countries.

Nichola J HawkinsDepartment of Biointeractions and Crop Protection, Rothamsted Research, Harpenden, AL5 4SE, U.K.ORCID https://orcid.org/0000-0003-3389-0436
Chris BassDepartment of Biosciences, University of Exeter, Penryn Campus, Cornwall, TR10 9FE, U.K.
Andrea DixonDepartment of Biointeractions and Crop Protection, Rothamsted Research, Harpenden, AL5 4SE, U.K.
Paul NeveDepartment of Biointeractions and Crop Protection, Rothamsted Research, Harpenden, AL5 4SE, U.K.
Rothamsted Research · GBUniversity of Exeter · GBUniversity of Georgia · US

Funding

Biotechnology and Biological Sciences Research Council BB/L001489/1BBS/OS/CP/000001European Research Council (ERC) 646625Strategic Longer and Larger (LoLa)
6 · The paper itself

Abstract

Durable crop protection is an essential component of current and future food security. However, the effectiveness of pesticides is threatened by the evolution of resistant pathogens, weeds and insect pests. Pesticides are mostly novel synthetic compounds, and yet target species are often able to evolve resistance soon after a new compound is introduced. Therefore, pesticide resistance provides an interesting case of rapid evolution under strong selective pressures, which can be used to address fundamental questions concerning the evolutionary origins of adaptations to novel conditions. We ask: (i) whether this adaptive potential originates mainly from de novo mutations or from standing variation; (ii) which pre-existing traits could form the basis of resistance adaptations; and (iii) whether recurrence of resistance mechanisms among species results from interbreeding and horizontal gene transfer or from independent parallel evolution. We compare and contrast the three major pesticide groups: insecticides, herbicides and fungicides. Whilst resistance to these three agrochemical classes is to some extent united by the common evolutionary forces at play, there are also important differences. Fungicide resistance appears to evolve, in most cases, by de novo point mutations in the target-site encoding genes; herbicide resistance often evolves through selection of polygenic metabolic resistance from standing variation; and insecticide resistance evolves through a combination of standing variation and de novo mutations in the target site or major metabolic resistance genes. This has practical implications for resistance risk assessment and management, and lessons learnt from pesticide resistance should be applied in the deployment of novel, non-chemical pest-control methods.

Indexed as

adaptive introgressionde novo mutationevolutionfungicideherbicideinsecticidepesticide resistancepleiotropic co-optionselective sweepsstanding variation

Identifiers

PMID29971903
PMCPMC6378405
OpenAlexW2810473995

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.