Evidence map›Paper›PMID 12586701›Full record

ArticleGenetics2003

Genetic analysis of Caenorhabditis elegans glp-1 mutants suggests receptor interaction or competition.

Anita S-R Pepper, Darrell J Killian, E Jane Albert Hubbard

Abstract read
In one paragraph

Article in Genetics, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

99 citing papers in PubMed, 153 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Biology · 2024
    Review
  9. LST-1 is a bifunctional regulator that feeds back on Notch-dependent transcription to regulateProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  10. Article
  11. Article
  12. Article
  13. Analysis of the C. elegans Germline Stem Cell Pool.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  14. Article
  15. MutantCancers · 2022
    Article
  16. Review
  17. A male pheromone that improves the quality of the oogenic germline.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  18. Laser Microdissection for Species-Agnostic Single-Tissue Applications.Journal of visualized experiments : JoVE · 2022
    Article
  19. Review
  20. Article

39 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

3 authors at 1 institution in 1 country.

Anita S-R PepperDepartment of Biology, New York University, New York, New York 10003, USA.
Darrell J Killian
E Jane Albert Hubbard
New York University · US

Funding

CONTROL ONSET OF MEIOSIS IN C. ELEGANSR01GM061706 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HUBBARD, E. JANE ALBERT · 2000 to 2018
$5.4M
TRAINING PROGRAM IN DEVELOPMENTAL GENETICS.T32HD007520 · NICHD · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI TREISMAN, JESSICA E · 1999 to 2023
$3.9M
NICHD NIH HHS T32HD07520NIGMS NIH HHS GM-61706NIGMS NIH HHS R01 GM061706
6 · The paper itself

Abstract

glp-1 encodes a member of the highly conserved LIN-12/Notch family of receptors that mediates the mitosis/meiosis decision in the C. elegans germline. We have characterized three mutations that represent a new genetic and phenotypic class of glp-1 mutants, glp-1(Pro). The glp-1(Pro) mutants display gain-of-function germline pattern defects, most notably a proximal proliferation (Pro) phenotype. Each of three glp-1(Pro) alleles encodes a single amino acid change in the extracellular part of the receptor: two in the LIN-12/Notch repeats (LNRs) and one between the LNRs and the transmembrane domain. Unlike other previously described gain-of-function mutations that affect this region of LIN-12/Notch family receptors, the genetic behavior of glp-1(Pro) alleles is not consistent with simple hypermorphic activity. Instead, the mutant phenotype is suppressed by wild-type doses of glp-1. Moreover, a trans-heterozygous combination of two highly penetrant glp-1(Pro) mutations is mutually suppressing. These results lend support to a model for a higher-order receptor complex and/or competition among receptor proteins for limiting factors that are required for proper regulation of receptor activity. Double-mutant analysis with suppressors and enhancers of lin-12 and glp-1 further suggests that the functional defect in glp-1(Pro) mutants occurs prior to or at the level of ligand interaction.

Indexed as

AnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsDNA-Binding ProteinsGlucagonGlucagon-Like Peptide 1Membrane ProteinsMutationPeptide FragmentsProtein PrecursorsReceptors, NotchSignal TransductionCaenorhabditis elegans ProteinsDNA-Binding ProteinsGlucagonGlucagon-Like Peptide 1LAG-1 protein, C eleganslag-2 protein, C elegansLin-12 protein, C elegansMembrane ProteinsPeptide FragmentsProtein PrecursorsReceptors, Notch

Identifiers

PMID12586701
PMCPMC1462416
OpenAlexW1961228933

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.