Evidence map›Paper›PMID 31307385›Full record

ArticleBMC bioinformatics2019

Stochastic modeling of aging cells reveals how damage accumulation, repair, and cell-division asymmetry affect clonal senescence and population fitness.

Ruijie Song, Murat Acar

Open access · goldAbstract read
In one paragraph

Article in BMC bioinformatics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

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  4. 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
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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

2 authors at 1 institution in 1 country.

Ruijie SongSystems Biology Institute, Yale University, 850 West Campus Drive, West Haven, CT, 06516, USA.
Murat AcarSystems Biology Institute, Yale University, 850 West Campus Drive, West Haven, CT, 06516, USA. murat.acar@yale.edu.
Yale University · US

Funding

Quantitative real-time characterization of single-cell aging: from phenotypes toDP2AG050461 · NIA · YALE UNIVERSITY · PI ACAR, MURAT · 2014 to 2014
$2.5M
Microfluids-enabled Quantitative Systems Biology Approaches to Construct Gene Networks Regulating Yeast Lifespan and Genetic Noise Dynamics During AgingR01GM127870 · NIGMS · YALE UNIVERSITY · PI ACAR, MURAT · 2018 to 2022
$1.5M
National Institute of General Medical Sciences (US) 1R01GM127870-01National Institute on Aging (US) 1DP2AG050461-01NIA NIH HHS DP2 AG050461NIGMS NIH HHS R01 GM127870
6 · The paper itself

Abstract

backgroundAsymmetry during cellular division, both in the uneven partitioning of damaged cellular components and of cell volume, is a cell biological phenomenon experienced by many unicellular organisms. Previous work based on a deterministic model claimed that such asymmetry in the partitioning of cell volume and of aging-associated damage confers a fitness benefit in avoiding clonal senescence, primarily by diversifying the cellular population. However, clonal populations of unicellular organisms are already naturally diversified due to the inherent stochasticity of biological processes.

resultsApplying a model of aging cells that accounts for natural cell-to-cell variations across a broad range of parameter values, here we show that the parameters directly controlling the accumulation and repair of damage are the most important factors affecting fitness and clonal senescence, while the effects of both segregation of damaged components and division asymmetry are frequently minimal and generally context-dependent.

conclusionsWe conclude that damage segregation and division asymmetry, perhaps counterintuitively, are not necessarily beneficial from an evolutionary perspective.

Indexed as

AgingModels, BiologicalAnimalsCell DivisionDNA DamageDNA RepairGerm CellsHumansStochastic Processes

Identifiers

PMID31307385
PMCPMC6631810
OpenAlexW2961272871

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.