ArticlemSystems2026
UV-B-induced DNA repair mechanisms and their effects on mutagenesis and culturability in
Article in mSystems, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- Accelerated Adaptive Evolution of Gram-Negative Bacteria With a Broad-Host-Range Dual Base Editor.Microbial biotechnology · 2026Article
- Article
- Biochemical and genomic characterization of last-resort antibiotic resistance and oxidant tolerance in environmentalFrontiers in toxicology · 2026Article
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3 authors.
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Abstract
Ultraviolet-B (UV-B) radiation, intensified by ozone depletion, induces DNA damage and promotes mutagenesis, shaping evolution. While UV-induced SOS responses are well characterized in bacteria, the cellular consequences of prolonged UV-B exposure remain less clear. Prolonged UV-B exposure disrupts transcription and translation, as well as RecA-mediated SOS induction, without major changes in membrane permeability or reactive oxygen species. This impairs mutagenesis and leads to an early loss of culturability. Genetic analysis reveals both redundant and differential roles for DNA repair pathways in which homologous recombination (RecA, RecB), nucleotide excision repair (UvrA), and translesion synthesis (UmuC/D) are essential for maintaining mutagenesis and culturability, while others (RecN, RmuC) have limited impact. Notably, deletion of UvrD (a repair-associated helicase) exacerbates the early impairment in culturability without affecting mutagenesis, underscoring the complexity of repair networks. Overall, our findings reveal a dose-dependent trade-off in which moderate UV-B promotes mutagenesis with minimal viability loss, whereas prolonged exposure suppresses mutagenesis with an early impairment in colony-forming ability, reflecting an adaptive strategy with significant evolutionary implications.IMPORTANCEUltraviolet radiation, especially UV-B, has shaped microbial evolution for billions of years by generating DNA lesions that activate mutagenic repair pathways. Because it induces both damage and adaptive responses, UV-B serves as a powerful model for examining how environmental stress influences genetic variation. While UV exposure is known to induce SOS-mediated DNA repair, its dual effects on mutagenesis and colony-forming ability are highly interconnected and complex, requiring further mechanistic analysis. This study provides insight into how prolonged UV-B exposure modulates these pathways, linking genetic responses with shifts in cellular states that influence culturability and mutagenic potential. Collectively, these findings can be highly informative for fundamental studies of microbial adaptation and for practical applications, where UV-B is used as a selective or perturbative tool, including biotechnology, directed evolution, and disinfection strategies.
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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.