Evidence map›Paper›PMID 29095106›Full record

ArticleFly2018

Deletion of the nicotinic acetylcholine receptor subunit gene Dα1 confers insecticide resistance, but at what cost?

Jason Somers, Hang Ngoc Bao Luong, Philip Batterham, Trent Perry

Open access · bronzeAbstract read
In one paragraph

Article in Fly, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

10 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Field-evolved resistance to neonicotinoids in the mosquito,bioRxiv : the preprint server for biology · 2024
    Article
  5. Article
  6. Article
  7. Temporal regulation of nicotinic acetylcholine receptor subunits supports central cholinergic synapse development inProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  8. The Power ofFrontiers in physiology · 2021
    Review
  9. Low doses of the neonicotinoid insecticide imidacloprid induce ROS triggering neurological and metabolic impairments inProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  10. The Neurotransmitters Involved inFrontiers in behavioral neuroscience · 2020
    Review
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 1 institution in 2 countries.

Jason Somersa School of BioSciences and Bio21 Molecular Science and Biotechnology Institute , University of Melbourne , Melbourne , VIC , Australia.
Hang Ngoc Bao Luonga School of BioSciences and Bio21 Molecular Science and Biotechnology Institute , University of Melbourne , Melbourne , VIC , Australia.
Philip Batterhama School of BioSciences and Bio21 Molecular Science and Biotechnology Institute , University of Melbourne , Melbourne , VIC , Australia.
Trent Perrya School of BioSciences and Bio21 Molecular Science and Biotechnology Institute , University of Melbourne , Melbourne , VIC , Australia.ORCID 0000-0002-8045-0487
The University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nicotinic acetylcholine receptors (nAChRs) have vital functions in processes of neurotransmission that underpin key behaviors. These pentameric ligand-gated ion channels have been used as targets for insecticides that constitutively activate them, causing the death of insect pests. In examining a knockout of the Dα1 nAChR subunit gene, our study linked this one subunit with multiple traits. We were able to confirm previous work that had identified Dα1 as a target of the neonicotinoid class of insecticides. Further, we uncovered roles for the gene in influencing mating behavior and patterns of sleep. The knockout mutant was also observed to have a significant reduction in longevity. This study highlighted the severe fitness costs that appear to be associated with the loss of function of this gene in natural populations in the absence of insecticides targeting the Dα1 subunit. Such a fitness cost could explain why target site resistances to neonicotinoids in pest insect populations have been associated specific amino acid replacement mutations in nAChR subunits, rather than loss of function. That mutant phenotypes were observed for the two behaviors examined indicates that the functions of Dα1, and other nAChR subunits, need to be explored more broadly. It also remains to be established whether these phenotypes were due to loss of the Dα1 receptor and/or to compensatory changes in the expression levels of other nAChR subunits.

Indexed as

Insecticide ResistanceAnimalsDrosophila melanogasterDrosophila ProteinsLife ExpectancyReceptors, NicotinicSexual Behavior, AnimalSleepDrosophila Proteinsnicotinic acetylcholine receptor alpha-subunits, DrosophilaReceptors, Nicotinicbehaviorcourtshipends-out gene targetinginsecticide resistancelongevitynicotinic acetylcholine receptor

Identifiers

PMID29095106
PMCPMC5927668
OpenAlexW2767075862

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.