UV-B-induced DNA repair mechanisms and their effects on mutagenesis and culturability in Escherichia coli
- 1William A. Brookshire Department of Chemical and Biomolecular Engineering, University of Houston, Houston, TX, USA
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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BibTeX
@article{ghosh2026uvbinduced,
title = {{UV-B-induced DNA repair mechanisms and their effects on mutagenesis and culturability in Escherichia coli}},
author = {Sreyashi Ghosh and Jenet Narzary and Mehmet A. Orman},
journal = {mSystems},
year = {2026},
month = jun,
doi = {10.1128/msystems.00396-26},
url = {https://doi.org/10.1128/msystems.00396-26},
note = {CC BY},
}
RIS
TY - JOUR
TI - UV-B-induced DNA repair mechanisms and their effects on mutagenesis and culturability in Escherichia coli
AU - Sreyashi Ghosh
AU - Jenet Narzary
AU - Mehmet A. Orman
PY - 2026
DA - 2026/06/12
JO - mSystems
DO - 10.1128/msystems.00396-26
UR - https://doi.org/10.1128/msystems.00396-26
AB - 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.
SN - 2379-5077
ER -