Evidence map›Paper›PMID 16802158›Full record

ArticleMolecular genetics and genomics : MGG2006

Wide mutational spectrum of a gene involved in hormone action and insecticide resistance in Drosophila melanogaster.

Thomas G Wilson, Shaoli Wang, Milan Beno, Robert Farkas

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular genetics and genomics : MGG, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Juvenile hormone regulates body size and perturbs insulin signaling in Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  5. Regulation of onset of female mating and sex pheromone production by juvenile hormone in Drosophila melanogaster.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Juvenile hormone resistance gene Methoprene-tolerant controls entry into metamorphosis in the beetle Tribolium castaneum.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
  12. Article
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 2 institutions in 2 countries.

Thomas G WilsonDepartment of Entomology, Ohio State University, Columbus, OH 43210, USA. wilson.1457@osu.edu
Shaoli Wang
Milan Beno
Robert Farkas
Institute of Experimental Endocrinology of the Slovak Academy of Sciences · SKThe Ohio State University · US

Funding

Juvenile Hormone Receptor in Flies and MosquitoesR01AI052290 · NIAID · OHIO STATE UNIVERSITY · PI WILSON, THOMAS G. · 2004 to 2007
$940k
Juvenile Hormone Receptor in Flies and MosquitoesR56AI052290 · NIAID · OHIO STATE UNIVERSITY · PI WILSON, THOMAS G. · 2010 to 2010
$229k
NIAID NIH HHS AI052290
6 · The paper itself

Abstract

The Methoprene-tolerant (Met) bHLH-PAS gene in Drosophila melanogaster is involved in the molecular action of juvenile hormone (JH), and mutants result in resistance to the toxic and morphogenetic effects of JH and JH agonist insecticides such as methoprene. A detailed study of Met mutants can shed light on the poorly understood action of JH as well as the molecular basis of Met resistance to JH insecticides. Nine mutant alleles bearing point mutations in Met were examined for penetrance and expressivity of three phenotypic characters: resistance, defective oogenesis, and a novel eye defect. The collection ranged from two weak alleles having less severe phenotypes to strong alleles with severe phenotypes similar to that of a null allele. The point mutations were located in both conserved and nonconserved domains. Both the eye defect, seen as severely malformed ommatidial facets in the posterior margin of the compound eye, and the oogenesis phenotype are nonconditional, whereas expression of the resistance phenotype requires treatment with JH or JH analogs (JHAs) during early metamorphosis. A proposed basis for all the phenotypic characters centers on MET action as a transcriptional regulator of ecdysone secondary-response target genes during metamorphosis. Disruption of MET function either by mutation or by JHA presence during early metamorphosis results in transcriptional misregulation of different target genes, resulting in the pathology seen in either instance. The variety of amino acid changes in MET that resulted in resistance may portend a rapid rise in resistance in response to increased use of JH insecticides in field insect populations.

Indexed as

AllelesAnimalsBasic Helix-Loop-Helix ProteinsDrosophila melanogasterDrosophila ProteinsEyeGenes, InsectInsecticide ResistanceMethopreneMutationOpen Reading FramesOvipositionPhenotypeBasic Helix-Loop-Helix ProteinsDrosophila ProteinsMethopreneMET protein, Drosophila

Identifiers

PMID16802158
OpenAlexW2088902512

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.