ArticleNature structural & molecular biology2024
The LexA-RecA* structure reveals a cryptic lock-and-key mechanism for SOS activation.
Article in Nature structural & molecular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Inhibition of the SOS response by olivetol improves the efficacy of DNA-damaging antibiotics in Escherichia coli.The Journal of antibiotics · 2026Article
- Genetic Code Expansion for Site-Specific Encoding of a Switchable, Intrinsic Fluorophore-Quencher Pair to Monitor Protein Dynamics.bioRxiv : the preprint server for biology · 2026Article
- Engineering a robust and autonomous biological funneling for efficient valorization of lignin-related aromatics.Nature communications · 2026Article
- A phage repressor involved in the DNA-damage response ofPNAS nexus · 2026Article
- Reclaiming the Microbial Battlefield: Adjuvant Strategies to Overcome Antibiotic Resistance.Microorganisms · 2026Review
- Mechanistic insights into the structure and function of the RecA C-terminal tail.Communications biology · 2026Article
- Rapid detection of genotoxicity employing an engineered high-sensitivity and tight SOS-response biosensor inSynthetic and systems biotechnology · 2026Article
- The Role of the Omega Subzone in Determining the Membership of a Protein in One of the Two Families of the LexA/Signal Peptidase-like Superfamily.International journal of molecular sciences · 2026Article
- Article
- Molecular basis of ampicillin resistance: combinatorial mechanisms and future strategies.World journal of microbiology & biotechnology · 2026Review
- Harnessing desiccation-tolerant cyanobacteria as biosensors for LexA-mediated responses in deep space.Frontiers in microbiology · 2026Article
- Identification and Characterization of a Small-Molecule Inhibitor of theACS infectious diseases · 2025Article
- Proteins need extra attention: improving the predictive power of protein language models on mutational datasets with hint tokens.NAR genomics and bioinformatics · 2025Article
- Adaptive Tolerance of Listeria monocytogenes to Chemical Oxidants: Comparative Analysis of Transcriptomic Studies.Comprehensive reviews in food science and food safety · 2025Review
- The conserved transcription factor PrlP modulates colonization and pathogenicity of Streptococcus suis in response to environmental stress.PLoS pathogens · 2025Article
- Synthesis and antimicrobial evaluation of a new hybrid bis-cyanoacrylamide-based-piperazine containing sulphamethoxazole moiety against rheumatoid arthritis-associated pathogens.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- SELECT: high-precision genome editing strategy via integration of CRISPR-Cas and DNA damage response for cross-species applications.Nucleic acids research · 2025Article
- Snapshots ofiScience · 2025Article
- Hallmarks of DNA replication stress responses in Escherichia coli and Bacillus subtilis.FEMS microbiology reviews · 2025Review
- The expression regulation ofFrontiers in microbiology · 2025Article
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Authors and funding
12 authors.
Funding
Abstract
The bacterial SOS response plays a key role in adaptation to DNA damage, including genomic stress caused by antibiotics. SOS induction begins when activated RecA*, an oligomeric nucleoprotein filament that forms on single-stranded DNA, binds to and stimulates autoproteolysis of the repressor LexA. Here, we present the structure of the complete Escherichia coli SOS signal complex, constituting full-length LexA bound to RecA*. We uncover an extensive interface unexpectedly including the LexA DNA-binding domain, providing a new molecular rationale for ordered SOS gene induction. We further find that the interface involves three RecA subunits, with a single residue in the central engaged subunit acting as a molecular key, inserting into an allosteric binding pocket to induce LexA cleavage. Given the pro-mutagenic nature of SOS activation, our structural and mechanistic insights provide a foundation for developing new therapeutics to slow the evolution of antibiotic resistance.
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