Evidence map›Paper›PMID 25419847›Full record

ArticleNature cell biology2014

DAF-16/FOXO and EGL-27/GATA promote developmental growth in response to persistent somatic DNA damage.

Michael M Mueller, Laia Castells-Roca, Vipin Babu, Maria A Ermolaeva, Roman-Ulrich Müller, Peter Frommolt, Ashley B Williams, Sebastian Greiss, Jennifer I Schneider, Thomas Benzing and 2 more

Open access · greenAbstract read
In one paragraph

Article in Nature cell biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

61 citing papers in PubMed, 108 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. DAF-16/FOXO maintains genome integrity following genotoxic stress.bioRxiv : the preprint server for biology · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Biomolecules · 2023
    Review
  15. FOXOs: masters of the equilibrium.The FEBS journal · 2022
    Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review

1 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

12 authors at 2 institutions in 1 country.

Michael M Mueller *Institute for Genome Stability in Ageing and Disease, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.
Laia Castells-Roca *Institute for Genome Stability in Ageing and Disease, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.
Vipin BabuInstitute for Genome Stability in Ageing and Disease, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.
Maria A ErmolaevaInstitute for Genome Stability in Ageing and Disease, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.
Roman-Ulrich MüllerCologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD) Research Center and Systems Biology of Ageing Cologne, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.
Peter FrommoltCologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD) Research Center and Systems Biology of Ageing Cologne, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.
Ashley B WilliamsInstitute for Genome Stability in Ageing and Disease, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.
Sebastian GreissCologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD) Research Center and Systems Biology of Ageing Cologne, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.
Jennifer I SchneiderInstitute for Genome Stability in Ageing and Disease, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.
Thomas BenzingCologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD) Research Center and Systems Biology of Ageing Cologne, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.
Bernhard SchermerCologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD) Research Center and Systems Biology of Ageing Cologne, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.
Björn SchumacherInstitute for Genome Stability in Ageing and Disease, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEUniversity of Cologne · DE

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
European Research Council 260383NIH HHS P40 OD010440NIH HHS P40OD010440
6 · The paper itself

Abstract

Genome maintenance defects cause complex disease phenotypes characterized by developmental failure, cancer susceptibility and premature ageing. It remains poorly understood how DNA damage responses function during organismal development and maintain tissue functionality when DNA damage accumulates with ageing. Here we show that the FOXO transcription factor DAF-16 is activated in response to DNA damage during development, whereas the DNA damage responsiveness of DAF-16 declines with ageing. We find that in contrast to its established role in mediating starvation arrest, DAF-16 alleviates DNA-damage-induced developmental arrest and even in the absence of DNA repair promotes developmental growth and enhances somatic tissue functionality. We demonstrate that the GATA transcription factor EGL-27 co-regulates DAF-16 target genes in response to DNA damage and together with DAF-16 promotes developmental growth. We propose that EGL-27/GATA activity specifies DAF-16-mediated DNA damage responses to enable developmental progression and to prolong tissue functioning when DNA damage persists.

Indexed as

AgingDNA DamageGene Expression Regulation, DevelopmentalAnimalsAnimals, Genetically ModifiedCaenorhabditis elegansCaenorhabditis elegans ProteinsDNA-Binding ProteinsDNA RepairForkhead Transcription FactorsHerbicidesParaquatSignal TransductionTranscription FactorsCaenorhabditis elegans Proteinsdaf-16 protein, C elegansDNA-Binding ProteinsEGL-27 protein, C elegansForkhead Transcription FactorsHerbicidesParaquatTranscription Factors

Identifiers

PMID25419847
PMCPMC4250074
OpenAlexW2094033379

What OpenQuestion holds

Textmetadata
LicenceTDM
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.