ArticleMolecular microbiology2025
In Vivo Nitrosative Stress-Induced Expression of a Photolyase Promotes Vibrio cholerae Environmental Blue Light Resistance.
Article in Molecular microbiology, 2025. 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.
- Role of photolyase in stress tolerance and virulence of plant-pathogenic bacteriumApplied and environmental microbiology · 2026Article
- Light-activated cAMP signaling controls sodium-driven motility inProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Nitric oxide promotes rapid development of motility to accelerate biofilm dispersal inProceedings of the National Academy of Sciences of the United States of America · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
Bacterial pathogens possess a remarkable capacity to sense and adapt to ever-changing environments. For example, Vibrio cholerae, the causative agent of the severe diarrheal disease cholera, thrives in aquatic ecosystems and human hosts through dynamic survival strategies. In this study, we investigated the role of three photolyases, enzymes that repair DNA damage caused by exposure to UV radiation and blue light, in the environmental survival of V. cholerae. Among these, we identified cry1 as critical for resistance to blue light, as mutations in this gene, but not in the other photolyase genes, rendered V. cholerae susceptible to such stress. Expression of cry1 was induced by blue light and regulated by RpoE and the anti-sigma factor ChrR. We further showed that nitric oxide (NO), a host-derived stressor encountered during infection, also activated cry1 expression. We found that one of the two cysteine residues in ChrR was important for sensing reactive nitrogen species (RNS), thereby modulating cry1 expression. While Cry1 was not required for V. cholerae colonization in animal models, pre-induction of Cry1 by RNS in vivo or in vitro enhanced V. cholerae resistance to blue light. These findings suggest that host-derived NO encountered during infection primes V. cholerae for survival in blue-light-rich aquatic environments, supporting its transition between host and environmental niches.
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