Evidence map›Paper›PMID 8807293›Full record

ArticleGenetics1996

Genetic analysis of the roles of daf-28 and age-1 in regulating Caenorhabditis elegans dauer formation.

E A Malone, T Inoue, J H Thomas

Abstract read
In one paragraph

Article in Genetics, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

51 citing papers in PubMed, 129 citations in OpenAlex.

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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.

E A MaloneDepartment of Genetics, University of Washington, Seattle 98195, USA.
T Inoue
J H Thomas
University of Washington · US

Funding

GENETIC ANALYSIS OF CHEMOSENSATION IN C ELEGANSR01GM048700 · NIGMS · UNIVERSITY OF WASHINGTON · PI THOMAS, JAMES H · 1993 to 2003
$1.2M
NIA NIH HHS AG-0057NIGMS NIH HHS R0GM48700
6 · The paper itself

Abstract

Based on environmental cues, the nervous system of Caenorhabditis elegans regulates formation of the dauer larva, an alternative larval form specialized for long-term survival under harsh conditions. Mutations that cause constitutive or defective dauer formation (Daf-c or Daf-d) have been identified and the genes ordered in a branched pathway. Most Daf-c mutations also affect recovery from the dauer stage. The semi-dominant mutation daf-28(sa191) is Daf-c but has no apparent effect on dauer recovery. We use this unique aspect of daf-28(sa191) to characterize the effects of several Daf-d and synthetic Daf-c mutations on dauer recovery. We present double mutant analysis that indicates that daf-28(sa191) acts at a novel point downstream in the genetic pathway for dauer formation. We also show that daf-28(sa191) causes a modest increase (12-13%) in life span. The phenotypes and genetic interactions of daf-28(sa191) are most similar to those of daf-2 and daf-23 mutations, which also cause a dramatic increase in life span. We present mapping and complementation data that suggest that daf-23 is the same gene as age-1, identified previously by mutations that extend life span. We find that age-1 alleles are also Daf-c at 27 degrees.

Indexed as

Epistasis, GeneticAllelesAnimalsCaenorhabditis elegansMutation

Identifiers

PMID8807293
PMCPMC1207390
OpenAlexW2134045835

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.