{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T05:39:08Z","timestamp":1790401148570,"version":"4.1.0"},"reference-count":44,"publisher":"American Society for Microbiology","issue":"11","license":[{"start":{"date-parts":[[2018,6,1]],"date-time":"2018-06-01T00:00:00Z","timestamp":1527811200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R21AI111018"],"award-info":[{"award-number":["R21AI111018"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Bacteriol"],"published-print":{"date-parts":[[2018,6]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Bacterial pathogenesis depends on changes in metabolic and virulence gene expression in response to changes within a pathogen's environment. The plague-causing pathogen,\n            <jats:named-content content-type=\"genus-species\">Yersinia pestis<\/jats:named-content>\n            , requires expression of the gene encoding the Pla protease for progression of pneumonic plague. The catabolite repressor protein Crp, a global transcriptional regulator, may serve as the activator of\n            <jats:italic>pla<\/jats:italic>\n            in response to changes within the lungs as disease progresses. By using gene reporter fusions, the spatial and temporal activation of the\n            <jats:italic>crp<\/jats:italic>\n            and\n            <jats:italic>pla<\/jats:italic>\n            promoters was measured in a mouse model of pneumonic plague. In the lungs,\n            <jats:italic>crp<\/jats:italic>\n            was highly expressed in bacteria found within large aggregates resembling biofilms, while\n            <jats:italic>pla<\/jats:italic>\n            expression increased over time independent of the aggregated state. Increased expression of\n            <jats:italic>crp<\/jats:italic>\n            and\n            <jats:italic>pla<\/jats:italic>\n            correlated with a reduction in lung glucose levels. Deletion of the glucose-specific phosphotransferase system EIIBC (PtsG) of\n            <jats:named-content content-type=\"genus-species\">Y. pestis<\/jats:named-content>\n            rescued glucose levels in the lungs, resulting in reduced expression of both\n            <jats:italic>crp<\/jats:italic>\n            and\n            <jats:italic>pla<\/jats:italic>\n            . We propose that activation of\n            <jats:italic>pla<\/jats:italic>\n            expression during pneumonic plague is driven by an increase of both Crp and cAMP levels following consumption of available glucose in the lungs by\n            <jats:named-content content-type=\"genus-species\">Y. pestis<\/jats:named-content>\n            . Thus, Crp operates as a sensor linking the nutritional environment of the host to regulation of virulence gene expression.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>IMPORTANCE<\/jats:bold>\n            Using\n            <jats:named-content content-type=\"genus-species\">Yersinia pestis<\/jats:named-content>\n            as a model for pneumonia, we discovered that glucose is rapidly consumed, leading to a catabolite-repressive environment in the lungs. As a result, expression of the gene encoding the plasminogen activator protease, a target of the catabolite repressor protein required for\n            <jats:named-content content-type=\"genus-species\">Y. pestis<\/jats:named-content>\n            pathogenesis, is activated. Interestingly, expression of the catabolite repressor protein itself was also increased in the absence of glucose but only in biofilms. The data presented here demonstrate how a bacterial pathogen senses changes within its environment to coordinate metabolism and virulence gene expression.\n          <\/jats:p>","DOI":"10.1128\/jb.00737-17","type":"journal-article","created":{"date-parts":[[2018,3,19]],"date-time":"2018-03-19T09:58:16Z","timestamp":1521453496000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":12,"title":["Depletion of Glucose Activates Catabolite Repression during Pneumonic Plague"],"prefix":"10.1128","volume":"200","author":[{"given":"Jeremy T.","family":"Ritzert","sequence":"first","affiliation":[{"name":"Department of Microbiology-Immunology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4347-089X","authenticated-orcid":false,"given":"Wyndham 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