ArticleNature communications2023
Damage dynamics and the role of chance in the timing of E. coli cell death.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
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- Compression of morbidity by interventions that steepen the survival curve.Nature communications · 2025Article
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- Dynamical Network Stability Analysis of Multiple Biological Ages Provides a Framework for Understanding the Aging Process.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Article
- Enhanced cellular longevity arising from environmental fluctuations.Cell systems · 2024Article
- Coinfecting phages impede each other's entry into the cell.Current biology : CB · 2024Article
- Scaling of stochastic growth and division dynamics: A comparative study of individual rod-shaped cells in the Mother Machine and SChemostat platforms.Molecular biology of the cell · 2024Article
- Nonlethal deleterious mutation-induced stress accelerates bacterial aging.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Gene expression tradeoffs determine bacterial survival and adaptation to antibiotic stress.bioRxiv : the preprint server for biology · 2024Article
- A brief overview of mathematical modeling of the within-host dynamics of Mycobacterium tuberculosis.Frontiers in applied mathematics and statistics · 2024Article
- Network dynamical stability analysis reveals key "mallostatic" natural variables that erode homeostasis and drive age-related decline of health.Scientific reports · 2023Article
- Transcriptional drift in aging cells: A global de-controller.bioRxiv : the preprint server for biology · 2023Article
- Single-cell patterning and characterisation of antibiotic persistent bacteria using bio-sCAPA.Lab on a chip · 2023Article
- PARROT: Prediction of enzyme abundances using protein-constrained metabolic models.PLoS computational biology · 2023Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetically identical cells in the same stressful condition die at different times. The origin of this stochasticity is unclear; it may arise from different initial conditions that affect the time of demise, or from a stochastic damage accumulation mechanism that erases the initial conditions and instead amplifies noise to generate different lifespans. To address this requires measuring damage dynamics in individual cells over the lifespan, but this has rarely been achieved. Here, we used a microfluidic device to measure membrane damage in 635 carbon-starved Escherichia coli cells at high temporal resolution. We find that initial conditions of damage, size or cell-cycle phase do not explain most of the lifespan variation. Instead, the data points to a stochastic mechanism in which noise is amplified by a rising production of damage that saturates its own removal. Surprisingly, the relative variation in damage drops with age: cells become more similar to each other in terms of relative damage, indicating increasing determinism with age. Thus, chance erases initial conditions and then gives way to increasingly deterministic dynamics that dominate the lifespan distribution.
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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.