In Vivo Nitrosative Stress-Induced Expression of a Photolyase Promotes Vibrio cholerae Environmental Blue Light Resistance

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.