Evidence map›Paper›PMID 25830239›Full record

ArticlePLoS genetics2015

Co-chaperone p23 regulates C. elegans Lifespan in Response to Temperature.

Makoto Horikawa, Surojit Sural, Ao-Lin Hsu, Adam Antebi

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 44 citations in OpenAlex.

  1. TheiScience · 2025
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  6. Organismal Roles of Hsp90.Biomolecules · 2023
    Review
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  8. NScience advances · 2021
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  18. The 4E-BP growth pathway regulates the effect of ambient temperature onProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  19. Article
  20. 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 4 institutions in 2 countries.

Makoto HorikawaMax Planck Institute for Biology of Ageing, Cologne, Germany.
Surojit SuralUniversity of Michigan, Department of Internal Medicine, Division of Geriatric and Palliative Medicine, Ann Arbor, Michigan, United States of America; University of Michigan, Department of Molecular and Integrative Physiology, Ann Arbor, Michigan, United States of America.
Ao-Lin HsuUniversity of Michigan, Department of Internal Medicine, Division of Geriatric and Palliative Medicine, Ann Arbor, Michigan, United States of America.
Adam AntebiMax Planck Institute for Biology of Ageing, Cologne, Germany; Cologne Excellence Cluster on Cellular Stress Responses in Ageing Associated Diseases (CECAD), University of Cologne, Cologne, Germany; Department of Molecular and Cellular Biology, Huffington Center on Ageing, Baylor College of Medicine, Houston, Texas, United States of America.
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEMax Planck Institute for Biology of Ageing · DEMichigan United · USUniversity of Michigan–Ann Arbor · US

Funding

Regulation of Heat Shock Transcription Factor in Long-lived AnimalsR01AG028516 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HSU, AO-LIN ALLEN · 2008 to 2017
$2.8M
NIA NIH HHS R01 AG028516
6 · The paper itself

Abstract

Temperature potently modulates various physiologic processes including organismal motility, growth rate, reproduction, and ageing. In ectotherms, longevity varies inversely with temperature, with animals living shorter at higher temperatures. Thermal effects on lifespan and other processes are ascribed to passive changes in metabolic rate, but recent evidence also suggests a regulated process. Here, we demonstrate that in response to temperature, daf-41/ZC395.10, the C. elegans homolog of p23 co-chaperone/prostaglandin E synthase-3, governs entry into the long-lived dauer diapause and regulates adult lifespan. daf-41 deletion triggers constitutive entry into the dauer diapause at elevated temperature dependent on neurosensory machinery (daf-10/IFT122), insulin/IGF-1 signaling (daf-16/FOXO), and steroidal signaling (daf-12/FXR). Surprisingly, daf-41 mutation alters the longevity response to temperature, living longer than wild-type at 25°C but shorter than wild-type at 15°C. Longevity phenotypes at 25°C work through daf-16/FOXO and heat shock factor hsf-1, while short lived phenotypes converge on daf-16/FOXO and depend on the daf-12/FXR steroid receptor. Correlatively daf-41 affected expression of DAF-16 and HSF-1 target genes at high temperature, and nuclear extracts from daf-41 animals showed increased occupancy of the heat shock response element. Our studies suggest that daf-41/p23 modulates key transcriptional changes in longevity pathways in response to temperature.

Indexed as

Heat-Shock ResponseLongevityAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCarrier ProteinsForkhead Transcription FactorsInsulin-Like Growth Factor IIntramolecular OxidoreductasesProstaglandin-E SynthasesSignal TransductionCaenorhabditis elegans ProteinsCarrier ProteinsDaf-10 protein, C elegansdaf-16 protein, C elegansForkhead Transcription FactorsInsulin-Like Growth Factor IIntramolecular OxidoreductasesProstaglandin-E Synthases

Identifiers

PMID25830239
PMCPMC4382338
OpenAlexW2080005377

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.