Evidence map›Paper›PMID 31120870›Full record

ArticlePLoS biology2019

Cell aging preserves cellular immortality in the presence of lethal levels of damage.

Audrey Menegaz Proenca, Camilla Ulla Rang, Andrew Qiu, Chao Shi, Lin Chao

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2019. 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
2.9field-weighted citation impact, top 9% 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, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. A link between aging and persistence.Antimicrobial agents and chemotherapy · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Talk to Me-Interplay between Mitochondria and Microbiota in Aging.International journal of molecular sciences · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Cellular senescence, rejuvenation and potential immortality.Proceedings. Biological sciences · 2022
    Review
  16. Review
  17. Review
  18. Asymmetry, division of labour and the evolution of ageing in multicellular organisms.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2021
    Review
  19. Article
  20. Nontraditional systems in aging research: an update.Cellular and molecular life sciences : CMLS · 2021
    Review
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

5 authors at 2 institutions in 2 countries.

Audrey Menegaz ProencaSection of Ecology, Behavior and Evolution, Division of Biological Sciences, University of California, San Diego, La Jolla, California, United States of America.ORCID 0000-0002-3747-9719
Camilla Ulla RangSection of Ecology, Behavior and Evolution, Division of Biological Sciences, University of California, San Diego, La Jolla, California, United States of America.
Andrew QiuSection of Ecology, Behavior and Evolution, Division of Biological Sciences, University of California, San Diego, La Jolla, California, United States of America.ORCID 0000-0003-4357-8622
Chao ShiSection of Ecology, Behavior and Evolution, Division of Biological Sciences, University of California, San Diego, La Jolla, California, United States of America.
Lin ChaoSection of Ecology, Behavior and Evolution, Division of Biological Sciences, University of California, San Diego, La Jolla, California, United States of America.
University of California San Diego · USMinistry of Education · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular aging, a progressive functional decline driven by damage accumulation, often culminates in the mortality of a cell lineage. Certain lineages, however, are able to sustain long-lasting immortality, as prominently exemplified by stem cells. Here, we show that Escherichia coli cell lineages exhibit comparable patterns of mortality and immortality. Through single-cell microscopy and microfluidic techniques, we find that these patterns are explained by the dynamics of damage accumulation and asymmetric partitioning between daughter cells. At low damage accumulation rates, both aging and rejuvenating lineages retain immortality by reaching their respective states of physiological equilibrium. We show that both asymmetry and equilibrium are present in repair mutants lacking certain repair chaperones, suggesting that intact repair capacity is not essential for immortal proliferation. We show that this growth equilibrium, however, is displaced by extrinsic damage in a dosage-dependent response. Moreover, we demonstrate that aging lineages become mortal when damage accumulation rates surpass a threshold, whereas rejuvenating lineages within the same population remain immortal. Thus, the processes of damage accumulation and partitioning through asymmetric cell division are essential in the determination of proliferative mortality and immortality in bacterial populations. This study provides further evidence for the characterization of cellular aging as a general process, affecting prokaryotes and eukaryotes alike and according to similar evolutionary constraints.

Indexed as

DNA DamageCell LineageCell PolarityCell ProliferationEscherichia coliEscherichia coli ProteinsMutationProtein AggregatesStress, PhysiologicalEscherichia coli ProteinsProtein Aggregates

Identifiers

PMID31120870
PMCPMC6532838
OpenAlexW2945020868

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.