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Zinc is an essential trace metal required for numerous cellular processes in all forms of life. In order to maintain zinc homeostasis, bacteria have developed several transport systems to regulate its uptake. In this study, we investigated zinc transport systems in the enteric pathogenVibrio cholerae , the causative agent of cholera. Bioinformatic analysis predicts that two gene clusters, VC2081 to VC2083 (annotated as zinc utilization genesznuABC ) and VC2551 to VC2555 (annotated asz inc-r egulatedg eneszrgABCDE ), are regulated by the putative zinc uptake regulator Zur. Using promoter reporter and biochemical assays, we confirmed that Zur repressesznuABC andzrgABCDE promoters in a Zn2+ -dependent manner. Under Zn2+ -limiting conditions, we found that mutations in either theznuABC orzrgABCDE gene cluster affect bacterial growth, withznuABC mutants displaying a more severe growth defect, suggesting that both ZnuABC and ZrgABCDE are involved in Zn2+ uptake and that ZnuABC plays the predominant role. Furthermore, we reveal that ZnuABC and ZrgABCDE are important forV. cholerae colonization in both infant and adult mouse models, particularly in the presence of other intestinal microbiota. Collectively, our studies indicate that these two zinc transporter systems play vital roles in maintaining zinc homeostasis duringV. cholerae growth and pathogenesis.

Dual Zinc Transporter Systems in Vibrio cholerae Promote Competitive Advantages over Gut Microbiome