Evidence map›Paper›PMID 27256978›Full record

ArticleOncotarget2016

Run-on of germline apoptosis promotes gonad senescence in C. elegans.

Yila de la Guardia, Ann F Gilliat, Josephine Hellberg, Peter Rennert, Filipe Cabreiro, David Gems

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.4field-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

46 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. TOCA-2 regulates gonad development inmicroPublication biology · 2026
    Article
  5. Review
  6. Apoptosis promotes fertility inbioRxiv : the preprint server for biology · 2025
    Article
  7. Article
  8. A hierarchy of causes of death in senescentbioRxiv : the preprint server for biology · 2025
    Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. AbioRxiv : the preprint server for biology · 2023
    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

6 authors at 2 institutions in 1 country.

Yila de la GuardiaInstitute of Healthy Ageing, and Department of Genetics, Evolution and Environment, University College London, London, UK.
Ann F GilliatInstitute of Healthy Ageing, and Department of Genetics, Evolution and Environment, University College London, London, UK.
Josephine HellbergInstitute of Healthy Ageing, and Department of Genetics, Evolution and Environment, University College London, London, UK.
Peter RennertInstitute of Healthy Ageing, and Department of Genetics, Evolution and Environment, University College London, London, UK.
Filipe CabreiroDepartment of Structural and Molecular Biology, University College London, London, UK.
David GemsInstitute of Healthy Ageing, and Department of Genetics, Evolution and Environment, University College London, London, UK.
University College London · GBInstitute of Structural and Molecular Biology · GB

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
NIH HHS P40 OD010440Wellcome Trust
6 · The paper itself

Abstract

Aging (senescence) includes causal mechanisms (etiologies) of late-life disease, which remain poorly understood. According to the recently proposed hyperfunction theory, based on the older theory of antagonistic pleiotropy, senescent pathologies can arise from futile, post-reproductive run-on of processes that in early life promote fitness. Here we apply this idea to investigate the etiology of senescent pathologies in the reproductive system of Caenorhabditis elegans hermaphrodites, particularly distal gonad degeneration and disintegration. Hermaphrodite germ cells frequently undergo "physiological" (non-damage-induced) apoptosis (PA) to provision growing oocytes. Run-on of such PA is a potential cause of age-related gonad degeneration. We document the continuation of germline apoptosis in later life, and report that genetically blocking or increasing PA retards or accelerates degeneration, respectively. In wild-type males, which lack germ line apoptosis, gonad disintegration does not occur. However, mutational induction of PA in males does not lead to gonad disintegration. These results suggest that as germ-cell proliferation rate declines markedly in aging hermaphrodites (but not males), run-on of PA becomes a pathogenic mechanism that promotes gonad degeneration. This illustrates how hyperfunction, or non-adaptive run-on in later life of a process that promotes fitness in early life, can promote atrophic senescent pathology in C. elegans.

Indexed as

AgingApoptosisAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCell ProliferationCellular SenescenceGerm CellsGonadsMaleMutationOocytesReceptor, InsulinRNA InterferenceSignal TransductionCaenorhabditis elegans ProteinsDAF-2 protein, C elegansReceptor, InsulinapoptosisC. elegansGerotargethyperfunctionpathologysenescence

Identifiers

PMID27256978
PMCPMC5129915
OpenAlexW2411016615

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.