{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T08:47:25Z","timestamp":1791103645571,"version":"4.1.0"},"reference-count":76,"publisher":"American Society for Microbiology","issue":"20","license":[{"start":{"date-parts":[[2011,10,15]],"date-time":"2011-10-15T00:00:00Z","timestamp":1318636800000},"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":["J Bacteriol"],"published-print":{"date-parts":[[2011,10,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Brucella melitensis<\/jats:named-content>\n            encounters a variety of conditions and stimuli during its life cycle\u2014including environmental growth, intracellular infection, and extracellular dissemination\u2014which necessitates flexibility of bacterial signaling to promote virulence. Cyclic-di-GMP is a bacterial secondary signaling molecule that plays an important role in adaptation to changing environments and altering virulence in a number of bacteria. To investigate the role of cyclic-di-GMP in\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. melitensis<\/jats:named-content>\n            , all 11 predicted cyclic-di-GMP-metabolizing proteins were separately deleted and the effect on virulence was determined. Three of these cyclic-di-GMP-metabolizing proteins were found to alter virulence. Deletion of the\n            <jats:italic>bpdA<\/jats:italic>\n            and\n            <jats:italic>bpdB<\/jats:italic>\n            genes resulted in attenuation of virulence of the bacterium, while deletion of the\n            <jats:italic>cgsB<\/jats:italic>\n            gene produced a hypervirulent strain. In a\n            <jats:italic>Vibrio<\/jats:italic>\n            reporter system to monitor apparent alteration in levels of cyclic-di-GMP, both BpdA and BpdB displayed a phenotype consistent with cyclic-di-GMP-specific phosphodiesterases, while CgsB displayed a cyclic-di-GMP synthase phenotype. Further analysis found that deletion of\n            <jats:italic>bpdA<\/jats:italic>\n            resulted in a dramatic decrease in flagellar promoter activities, and a flagellar mutant showed similar phenotypes to the\n            <jats:italic>bpdA<\/jats:italic>\n            and\n            <jats:italic>bpdB<\/jats:italic>\n            mutant strains in mouse models of infection. These data indicate a potential role for regulation of flagella in\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Brucella melitensis<\/jats:named-content>\n            via cyclic-di-GMP.\n          <\/jats:p>","DOI":"10.1128\/jb.00428-11","type":"journal-article","created":{"date-parts":[[2011,8,20]],"date-time":"2011-08-20T02:30:05Z","timestamp":1313807405000},"page":"5683-5691","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":40,"title":["Brucella melitensis Cyclic di-GMP Phosphodiesterase BpdA Controls Expression of Flagellar Genes"],"prefix":"10.1128","volume":"193","author":[{"given":"Erik","family":"Petersen","sequence":"first","affiliation":[{"name":"Department of Pathobiological Sciences, University of Wisconsin\u2014Madison, 1656 Linden Dr., Madison, Wisconsin 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