ArticleNucleic acids research2021
Cellular heterogeneity in DNA alkylation repair increases population genetic plasticity.
Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- A self-iterative orthogonal base-editing platform enables multiplex N-to-N diversification and genome-scale functional screening in Escherichia coli.Nucleic acids research · 2026Article
- Pangenomic and genomic plasticity analyses of the genus Rickettsia.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2026Article
- Periplasmic detoxification of urate hydroperoxide underpinsbioRxiv : the preprint server for biology · 2026Article
- Suppression of bacterial cell death underlies the antagonistic interaction between ciprofloxacin and tetracycline.Molecular systems biology · 2026Article
- Estimating mutation rates under heterogeneous stress responses.PLoS computational biology · 2024Article
- Article
- Phenotypic heterogeneity in the bacterial oxidative stress response is driven by cell-cell interactions.Cell reports · 2023Article
- Adaptation delay causes a burst of mutations in bacteria responding to oxidative stress.EMBO reports · 2023Article
- Microfluidics for long-term single-cell time-lapse microscopy: Advances and applications.Frontiers in bioengineering and biotechnology · 2022Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
DNA repair mechanisms fulfil a dual role, as they are essential for cell survival and genome maintenance. Here, we studied how cells regulate the interplay between DNA repair and mutation. We focused on the adaptive response that increases the resistance of Escherichia coli cells to DNA alkylation damage. Combination of single-molecule imaging and microfluidic-based single-cell microscopy showed that noise in the gene activation timing of the master regulator Ada is accurately propagated to generate a distinct subpopulation of cells in which all proteins of the adaptive response are essentially absent. Whereas genetic deletion of these proteins causes extreme sensitivity to alkylation stress, a temporary lack of expression is tolerated and increases genetic plasticity of the whole population. We demonstrated this by monitoring the dynamics of nascent DNA mismatches during alkylation stress as well as the frequency of fixed mutations that are generated by the distinct subpopulations of the adaptive response. We propose that stochastic modulation of DNA repair capacity by the adaptive response creates a viable hypermutable subpopulation of cells that acts as a source of genetic diversity in a clonal population.
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