ArticleScience (New York, N.Y.)2012
Identity and function of a large gene network underlying mutagenic repair of DNA breaks.
Article in Science (New York, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.
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Who cites it
137 citing papers in PubMed.
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- "Excluded phenotypes" restrict genetic paths toward adaptation in declining populations.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Enhancing the heat tolerance of homolactic Escherichia coli through reverse metabolic engineering.Applied microbiology and biotechnology · 2026Article
- Consequences of benzalkonium chloride tolerance for selection dynamics and de novo resistance evolution driven by antibiotics.npj antimicrobials and resistance · 2026Article
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- Azithromycin represses evolution of ceftazidime/avibactam resistance by translational repression ofJournal of bacteriology · 2025Article
- Rapid identification of key antibiotic resistance genes iniScience · 2025Article
- The Emerging Role of (p)ppGpp in DNA Repair and Associated Bacterial Survival against Fluoroquinolones.Gene expression · 2025Article
- Pathogen-encoded Rum DNA polymerase drives rapid bacterial drug resistance.Nucleic acids research · 2024Article
- Drug tolerant persister cell plasticity in cancer: A revolutionary strategy for more effective anticancer therapies.Signal transduction and targeted therapy · 2024Review
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- The F plasmid conjutome: the repertoire ofmSphere · 2024Article
- Bacterial persisters: molecular mechanisms and therapeutic development.Signal transduction and targeted therapy · 2024Review
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- High-Throughput Screening Method UsingMicroorganisms · 2024Article
- Trade-offs, trade-ups, and high mutational parallelism underlie microbial adaptation during extreme cycles of feast and famine.Current biology : CB · 2024Article
77 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Mechanisms of DNA repair and mutagenesis are defined on the basis of relatively few proteins acting on DNA, yet the identities and functions of all proteins required are unknown. Here, we identify the network that underlies mutagenic repair of DNA breaks in stressed Escherichia coli and define functions for much of it. Using a comprehensive screen, we identified a network of ≥93 genes that function in mutation. Most operate upstream of activation of three required stress responses (RpoS, RpoE, and SOS, key network hubs), apparently sensing stress. The results reveal how a network integrates mutagenic repair into the biology of the cell, show specific pathways of environmental sensing, demonstrate the centrality of stress responses, and imply that these responses are attractive as potential drug targets for blocking the evolution of pathogens.
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Registered trials
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