{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T23:50:01Z","timestamp":1789948201972,"version":"4.0.1"},"reference-count":43,"publisher":"American Society for Microbiology","issue":"10","license":[{"start":{"date-parts":[[2015,10,1]],"date-time":"2015-10-01T00:00:00Z","timestamp":1443657600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2015,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            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 pathogen\n            <jats:named-content content-type=\"genus-species\">Vibrio cholerae<\/jats:named-content>\n            , the causative agent of cholera. Bioinformatic analysis predicts that two gene clusters, VC2081 to VC2083 (annotated as zinc utilization genes\n            <jats:italic>znuABC<\/jats:italic>\n            ) and VC2551 to VC2555 (annotated as\n            <jats:underline>z<\/jats:underline>\n            inc-\n            <jats:underline>r<\/jats:underline>\n            egulated\n            <jats:underline>g<\/jats:underline>\n            enes\n            <jats:italic>zrgABCDE<\/jats:italic>\n            ), are regulated by the putative zinc uptake regulator Zur. Using promoter reporter and biochemical assays, we confirmed that Zur represses\n            <jats:italic>znuABC<\/jats:italic>\n            and\n            <jats:italic>zrgABCDE<\/jats:italic>\n            promoters in a Zn\n            <jats:sup>2+<\/jats:sup>\n            -dependent manner. Under Zn\n            <jats:sup>2+<\/jats:sup>\n            -limiting conditions, we found that mutations in either the\n            <jats:italic>znuABC<\/jats:italic>\n            or\n            <jats:italic>zrgABCDE<\/jats:italic>\n            gene cluster affect bacterial growth, with\n            <jats:italic>znuABC<\/jats:italic>\n            mutants displaying a more severe growth defect, suggesting that both ZnuABC and ZrgABCDE are involved in Zn\n            <jats:sup>2+<\/jats:sup>\n            uptake and that ZnuABC plays the predominant role. Furthermore, we reveal that ZnuABC and ZrgABCDE are important for\n            <jats:named-content content-type=\"genus-species\">V. cholerae<\/jats:named-content>\n            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 during\n            <jats:named-content content-type=\"genus-species\">V. cholerae<\/jats:named-content>\n            growth and pathogenesis.\n          <\/jats:p>","DOI":"10.1128\/iai.00447-15","type":"journal-article","created":{"date-parts":[[2015,7,21]],"date-time":"2015-07-21T02:04:50Z","timestamp":1437444290000},"page":"3902-3908","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":47,"title":["Dual Zinc Transporter Systems in Vibrio cholerae Promote Competitive Advantages over Gut Microbiome"],"prefix":"10.1128","volume":"83","author":[{"given":"Ying","family":"Sheng","sequence":"first","affiliation":[{"name":"Department of Microbiology, Nanjing Agricultural University, Nanjing, China"},{"name":"State Key Laboratory for Infectious Disease Prevention and Control, National Institute for 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