Evidence map›Paper›PMID 38787879›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2024

Balance between asymmetric allocation and repair of somatic damage in unicellular life forms as an ancient form of r/K selection.

Dmitry A Biba, Yuri I Wolf, Eugene V Koonin, Nash D Rochman

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Why did some viruses evolve to be giants while others did not?Proceedings of the National Academy of Sciences of the United States of America · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors.

Dmitry A BibaNational Center for Biotechnology Information, National Library of Medicine, NIH, Bethesda, MD 20894.
Yuri I WolfNational Center for Biotechnology Information, National Library of Medicine, NIH, Bethesda, MD 20894.ORCID 0000-0002-0247-8708
Eugene V KooninNational Center for Biotechnology Information, National Library of Medicine, NIH, Bethesda, MD 20894.ORCID 0000-0003-3943-8299
Nash D RochmanNational Center for Biotechnology Information, National Library of Medicine, NIH, Bethesda, MD 20894.

Funding

HHS | National Institutes of Health (NIH) Intramural Research Program
6 · The paper itself

Abstract

Over the course of multiple divisions, cells accumulate diverse nongenetic, somatic damage including misfolded and aggregated proteins and cell wall defects. If the rate of damage accumulation exceeds the rate of dilution through cell growth, a dedicated mitigation strategy is required to prevent eventual population collapse. Strategies for somatic damage control can be divided into two categories, asymmetric allocation and repair, which are not, in principle, mutually exclusive. We explore a mathematical model to identify the optimal strategy, maximizing the total cell number, over a wide range of environmental and physiological conditions. The optimal strategy is primarily determined by extrinsic, damage-independent mortality and the physiological model for damage accumulation that can be either independent (linear) or increasing (exponential) with respect to the prior accumulated damage. Under the linear regime, the optimal strategy is either exclusively repair or asymmetric allocation, whereas under the exponential regime, the optimal strategy is a combination of asymmetry and repair. Repair is preferred when extrinsic mortality is low, whereas at high extrinsic mortality, asymmetric damage allocation becomes the strategy of choice. We hypothesize that at an early stage of life evolution, optimization over repair and asymmetric allocation of somatic damage gave rise to

Indexed as

Models, BiologicalBiological EvolutionSelection, Geneticasymmetric cell divisionasymmetric damage allocationr and K selectionsomatic damage accumulationsomatic damage repair

Identifiers

PMID38787879
PMCPMC11145259

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.