Evidence map›Paper›PMID 25184818›Full record

ArticleBMC biology2014

Repair rather than segregation of damage is the optimal unicellular aging strategy.

Robert J Clegg, Rosemary J Dyson, Jan-Ulrich Kreft

Abstract read
In one paragraph

Article in BMC biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Balance between asymmetric allocation and repair of somatic damage in unicellular life forms as an ancient form of r/K selection.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  2. Article
  3. Article
  4. Cellular senescence, rejuvenation and potential immortality.Proceedings. Biological sciences · 2022
    Review
  5. Review
  6. Senescence in Bacteria and Its Underlying Mechanisms.Frontiers in cell and developmental biology · 2021
    Review
  7. Article
  8. Article
  9. Review
  10. Protein aggregation in bacteria.FEMS microbiology reviews · 2020
    Review
  11. Microbial ageing and longevity.Nature reviews. Microbiology · 2019
    Review
  12. Review
  13. Modelling the host-pathogen interactions of macrophages andJournal of the Royal Society, Interface · 2017
    Article
  14. Review
  15. Article
  16. Review
  17. 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.

Robert J Clegg
Rosemary J Dyson
Jan-Ulrich KreftCentre for Systems Biology, University of Birmingham, Birmingham, UK. j.kreft@bham.ac.uk.

Funding

National Centre for the Replacement, Refinement and Reduction of Animals in Research NC/K000683/1
6 · The paper itself

Abstract

backgroundHow aging, being unfavourable for the individual, can evolve is one of the fundamental problems of biology. Evidence for aging in unicellular organisms is far from conclusive. Some studies found aging even in symmetrically dividing unicellular species; others did not find aging in the same, or in different, unicellular species, or only under stress. Mathematical models suggested that segregation of non-genetic damage, as an aging strategy, would increase fitness. However, these models failed to consider repair as an alternative strategy or did not properly account for the benefits of repair. We used a new and improved individual-based model to examine rigorously the effect of a range of aging strategies on fitness in various environments.

resultsRepair of damage emerges as the best strategy despite its fitness costs, since it immediately increases growth rate. There is an optimal investment in repair that outperforms damage segregation in well-mixed, lasting and benign environments over a wide range of parameter values. Damage segregation becomes beneficial, and only in combination with repair, when three factors are combined: (i) the rate of damage accumulation is high, (ii) damage is toxic and (iii) efficiency of repair is low. In contrast to previous models, our model predicts that unicellular organisms should have active mechanisms to repair damage rather than age by segregating damage. Indeed, as predicted, all organisms have evolved active mechanisms of repair whilst aging in unicellular organisms is absent or minimal under benign conditions, apart from microorganisms with a different ecology, inhabiting short-lived environments strongly favouring early reproduction rather than longevity.

conclusionsAging confers no fitness advantage for unicellular organisms in lasting environments under benign conditions, since repair of non-genetic damage is better than damage segregation.

Indexed as

AgingModels, BiologicalBacteriaDNA DamageDNA RepairMicrobial Viability

Identifiers

PMID25184818
PMCPMC4243282

What OpenQuestion holds

Textmetadata
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.