ArticlePLoS genetics2010
A model for damage load and its implications for the evolution of bacterial aging.
Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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.
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.
Who cites it
28 citing papers in PubMed.
- Article
- Protein aggregation as a bistable switch in bacterial cell fate: from adaptive dormancy to cytotoxic death.Frontiers in microbiology · 2026Review
- Computational Systems Biology Approaches to Cellular Aging - Integrating Network Maps and Dynamical Models.Quantitative biology (Beijing, China) · 2025Article
- A link between aging and persistence.Antimicrobial agents and chemotherapy · 2025Article
- Article
- Progressive decline in old pole gene expression signal enhances phenotypic heterogeneity in bacteria.Science advances · 2024Article
- 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 · 2024Article
- Unicellular life balances asymmetric allocation and repair of somatic damage representing the origin of r/K selection.bioRxiv : the preprint server for biology · 2023Article
- Interacting bactofilins impact cell shape of the MreB-less multicellular Rhodomicrobium vannielii.PLoS genetics · 2023Article
- Modeling aging and its impact on cellular function and organismal behavior.Experimental gerontology · 2021Review
- Survival of the first rather than the fittest in a Shewanella electrode biofilm.Communications biology · 2021Article
- Senescence in Bacteria and Its Underlying Mechanisms.Frontiers in cell and developmental biology · 2021Review
- Article
- The synergy of damage repair and retention promotes rejuvenation and prolongs healthy lifespans in cell lineages.PLoS computational biology · 2020Article
- Allocation of gene products to daughter cells is determined by the age of the mother in singleProceedings. Biological sciences · 2020Article
- Bacterial ageing in the absence of external stressors.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Article
- Microbial ageing and longevity.Nature reviews. Microbiology · 2019Review
- Cell aging preserves cellular immortality in the presence of lethal levels of damage.PLoS biology · 2019Article
- Evolutionary model for the unequal segregation of high copy plasmids.PLoS computational biology · 2019Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deleterious mutations appearing in a population increase in frequency until stopped by natural selection. The ensuing equilibrium creates a stable frequency of deleterious mutations or the mutational load. Here I develop the comparable concept of a damage load, which is caused by harmful non-heritable changes to the phenotype. A damage load also ensues when the increase of damage is opposed by selection. The presence of a damage load favors the evolution of asymmetrical transmission of damage by a mother to her daughters. The asymmetry is beneficial because it increases fitness variance, but it also leads to aging or senescence. A mathematical model based on microbes reveals that a cell lineage dividing symmetrically is immortal if lifetime damage rates do not exceed a threshold. The evolution of asymmetry allows the lineage to persist above the threshold, but the lineage becomes mortal. In microbes with low genomic mutation rates, it is likely that the damage load is much greater than the mutational load. In metazoans with higher genomic mutation rates, the damage and the mutational load could be of the same magnitude. A fit of the model to experimental data shows that Escherichia coli cells experience a damage rate that is below the threshold and are immortal under the conditions examined. The model estimates the asymmetry level of E. coli to be low but sufficient for persisting at higher damage rates. The model also predicts that increasing asymmetry results in diminishing fitness returns, which may explain why the bacterium has not evolved higher asymmetry.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.