ArticleNature communications2025
Lineage-dependent variations in single-cell antibiotic susceptibility reveal the selective inheritance of phenotypic resistance in bacteria.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed.
- Bacterial heteroresistance mechanisms, dynamics, and emerging diagnostic approaches.Bioscience reports · 2026Review
- Heterogeneity in microbial antibiotic responses: genetic basis and within-host evolution.Trends in genetics : TIG · 2026Review
- Beyond resistance and tolerance: rethinking evolutionary responses to antibiotics from the perspective of individual bacterial cells.Nature communications · 2026Review
- High-resolution, high-throughput detection of hidden antibiotic resistance with the dilution-and-delay (DnD) susceptibility assay.Nature communications · 2026Article
- Cell-to-Cell and Patient-to-Patient Variability in Antimicrobial Resistance.Microorganisms · 2025Review
- Isolation, Identification, and Antibiotic Resistance, CRISPR System Analysis ofMicroorganisms · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Genetically identical bacterial cells often exhibit heterogeneous responses to antibiotics - some survive, others die. Here, we show that this heterogeneity propagates across generations to give rise to phenotypic resistance. Using real-time single-cell tracking, we exposed Escherichia coli to the β-lactam cefsulodin at its clinical breakpoint concentration and analyzed cell fate within genealogical trees statistically. Cell survival was strongly correlated among family members, driving the selective enrichment of robust lineages within an otherwise susceptible population. Our genealogical population model identified heritable phenotypic resistance as a key factor underlying this enrichment, which was validated experimentally. Comparing enrichment dynamics between the wild-type and a tolC knock-out strain, deficient in multidrug efflux, uncovered nuanced changes that increased the intergenerational memory of phenotypic resistance. Our findings provide evidence for heritable phenotypic resistance and demonstrate how its propagation through cell-to-cell heterogeneity enables the survival of minority cells within isogenic populations.
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Registered trials
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