Light-activated cAMP signaling controls sodium-driven motility in <i>Vibrio cholerae</i>.

Abstract

Light is one of the most pervasive physical cues in aquatic environments, yet its impact on nonphototrophic pathogens remains largely unexplored. Here, we show that a strain of cholera bacterium <i>Vibrio cholerae</i> directly couples illumination to motility through cyclic AMP (cAMP) signaling. Exposure to visible light rapidly elevates intracellular cAMP and increases swimming speed, whereas deletion of the single adenylyl cyclase gene (<i>cyaA</i>) abolishes both responses; complementation or addition of exogenous cAMP restores the phenotype. Heterologous expression of <i>V. cholerae</i> CyaA in an <i>Escherichia coli</i> Δ<i>cyaA</i> Δ<i>cpdA</i> background reconstitutes light-activated cAMP synthesis, indicating that CyaA confers photoreactivity. Purified CyaA exhibits a reversible light-dependent spectral shift consistent with flavin-dependent photochemistry, identifying it as a light-responsive cyclase. Illumination triggers rapid membrane hyperpolarization and sodium efflux, strengthening the sodium-motive force that powers the flagellar motor. This response persists under nutrient-limited conditions. Together, these findings define a light → cAMP → sodium-motive force coupling axis in <i>V. cholerae</i>, suggesting that ambient light may influence motility and dispersal in sunlit environments.