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.