Summary
Bacterial pathogens possess the remarkable ability to sense and adapt to
their constantly changing environments. For example, Vibrio
cholerae , the causative agent of the severe diarrheal disease cholera,
thrives in aquatic settings and infects human hosts, employing dynamic
strategies to ensure survival between diverse environments. In this
study, we utilized RNA sequencing to investigate how V.
cholerae responds to nitric oxide (NO), a common stressor encountered
during infection. We found that cry1 , encoding a photolyase,
which repairs DNA damage caused by exposure to blue light—a stressor
found in aquatic environments—was induced by NO. We observed thatcry1 was activated upon exposure to blue light and Cry1
contributed to mitigating blue light-induced reactive oxygen species
(ROS) production and stress responses. Cry1 is important for
protecting cells against blue light-induced cell death. Furthermore, we
showed that pre-induced Cry1 production, either by exposure to reactive
nitrogen species (RNS) in vitro or in mice, enhanced V.
cholerae ’s resistance to blue light. Additionally, we found
that V. cholerae Cry1 and the E. coli ortholog PhrB were
crucial in resisting reactive oxygen species (ROS).
Moreover, cry1 expression was regulated by RpoE and the
anti-sigma factor ChrR, with two cysteine residues in ChrR playing vital
roles in sensing RNS and blue light-induced ROS, thereby
modulating cry1 expression. Collectively, our findings suggest
that V. cholerae encounters host-derived NO during infection, and
the subsequent induction of Cry1 primes the bacterium effectively for
challenges in aquatic environments abundant in blue light once it exits
the host gut.