Evidence map›Paper›PMID 42283459›Full record

ArticlemSystems2026

UV-B-induced DNA repair mechanisms and their effects on mutagenesis and culturability in

Sreyashi Ghosh, Jenet Narzary, Mehmet A Orman

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Life (Basel, Switzerland) · 2026
    Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Sreyashi GhoshDepartment of Chemical and Biomolecular Engineering, University of Houston, Houston, Texas, USA.ORCID 0000-0002-0346-7381
Jenet NarzaryDepartment of Chemical and Biomolecular Engineering, University of Houston, Houston, Texas, USA.ORCID 0009-0009-5101-8044
Mehmet A OrmanDepartment of Chemical and Biomolecular Engineering, University of Houston, Houston, Texas, USA.ORCID 0000-0001-8499-9154

Funding

Characterizing a Self-Digesting-Mediated Reversible Drug Tolerance Mechanism in BacteriaR01AI143643 · NIAID · UNIVERSITY OF HOUSTON · PI ORMAN, MEHMET A. · 2020 to 2024
$1.9M
National Institute of Allergy and Infectious Diseases R01-AI143643National Science Foundation 2326142NIAID NIH HHS R01 AI143643
6 · The paper itself

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.

Indexed as

DNA RepairEscherichia coliMutagenesisUltraviolet RaysDNA DamageEscherichia coli ProteinsExcision RepairSOS Response, GeneticsTranslesion DNA SynthesisEscherichia coli Proteinscolony-forming abilityDNA repairEscherichia colimutagenesisSOS responseultraviolet-B

Identifiers

PMID42283459
PMCPMC13386880

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LicenceCC BY
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Registered trials

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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.