Evidence map›Paper›PMID 25702753›Full record

ArticleAging cell2015

Evidence that mutation accumulation does not cause aging in Saccharomyces cerevisiae.

Alaattin Kaya, Alexei V Lobanov, Vadim N Gladyshev

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.6field-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

38 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Molecular Damage in Aging.Nature aging · 2021
    Review
  12. Review
  13. Review
  14. The Evolution of the Hallmarks of Aging.Frontiers in genetics · 2021
    Review
  15. Transcriptomic and genomic changes associated with radioadaptation inComputational and structural biotechnology journal · 2021
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Defining the impact of mutation accumulation on replicative lifespan in yeast using cancer-associated mutator phenotypes.Proceedings of the National Academy of Sciences of the United States of America · 2019
    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

3 authors at 2 institutions in 1 country.

Alaattin KayaDivision of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
Alexei V Lobanov
Vadim N Gladyshev
Harvard University · USBrigham and Women's Hospital · US

Funding

Functions of thioredoxin reductases and their targetsR37GM065204 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI GLADYSHEV, VADIM N. · 2011 to 2020
$4.0M
Functions of Mammalian Thioredoxin ReductasesR01GM065204 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI GLADYSHEV, VADIM N. · 2002 to 2009
$2.2M
Understanding the Causes of AgingR01AG038004 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI GLADYSHEV, VADIM N. · 2010 to 2013
$1.1M
NIA NIH HHS AG038004NIGMS NIH HHS GM065204NIGMS NIH HHS R37 GM065204
6 · The paper itself

Abstract

The concept that mutations cause aging phenotypes could not be directly tested previously due to inability to identify age-related mutations in somatic cells and determine their impact on organismal aging. Here, we subjected Saccharomyces cerevisiae to multiple rounds of replicative aging and assessed de novo mutations in daughters of mothers of different age. Mutations did increase with age, but their low numbers, < 1 per lifespan, excluded their causal role in aging. Structural genome changes also had no role. A mutant lacking thiol peroxidases had the mutation rate well above that of wild-type cells, but this did not correspond to the aging pattern, as old wild-type cells with few or no mutations were dying, whereas young mutant cells with many more mutations continued dividing. In addition, wild-type cells lost mitochondrial DNA during aging, whereas shorter-lived mutant cells preserved it, excluding a causal role of mitochondrial mutations in aging. Thus, DNA mutations do not cause aging in yeast. These findings may apply to other damage types, suggesting a causal role of cumulative damage, as opposed to individual damage types, in organismal aging.

Indexed as

Mutation AccumulationDNA, MitochondrialMitochondriaMutationMutation RateSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsDNA, MitochondrialSaccharomyces cerevisiae ProteinsagingDNA damagelifespanmitochondriamutationsthiol peroxidaseyeast

Identifiers

PMID25702753
PMCPMC4406665
OpenAlexW2164454836

What OpenQuestion holds

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LicenceCC BY
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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.