Conclusion
In this study, we discovered that in V. cholerae , Cry1, which is
known for repairing DNA damage caused by blue light, can also be
activated by signals from the host-derived nitric oxide. The
physiological significance of this regulation is proposed in the
following working model (Fig. 6). V. cholerae manifests itself
through two distinct lifestyles: one entails the colonization of a host
organism, while the other involves its habitation within aquatic
ecosystems. During the course of infection, the host’s production of
reactive nitrogen species (RNS) orchestrates a modification of the ChrR
protein, prompting its dissociation from RpoE. This leads to the
activation of RpoE, which in turn triggers the transcriptional
upregulation of cry1 . Upon exiting from the host environments,V. cholerae exhibits enhanced resilience within aquatic habitats,
where encounters with blue light and an array of reactive oxygen species
are prevalent. This heightened resilience is attributed to the
preinduction of Cry1 facilitated by the earlier exposure to host-derived
signals. This adaptive mechanism bestows V. cholerae with an
amplified fitness advantage, bolstering its adaptability and success
within aquatic environments. The multifaceted interplay of these
regulatory processes underscores the dynamic strategies employed byV. cholerae to thrive under diverse conditions.