{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T01:45:20Z","timestamp":1789436720930,"version":"build-2803163510"},"reference-count":36,"publisher":"American Society for Microbiology","issue":"13","license":[{"start":{"date-parts":[[2012,7,1]],"date-time":"2012-07-01T00:00:00Z","timestamp":1341100800000},"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":[[2012,7]]},"abstract":"ABSTRACT<\/jats:title>\n \n The Entner-Doudoroff (ED) pathway has recently been shown to play an important role in sugar catabolism for many organisms although very little information is available on the functionality of this pathway in\n Vibrio cholerae<\/jats:named-content>\n , the causative agent of cholera. In this study, activation of the genes\n edd<\/jats:italic>\n and\n eda<\/jats:italic>\n , encoding 6-phosphogluconate dehydratase and 2-keto-3-deoxy-6-phosphogluconate aldolase, was used as a marker of a functional ED pathway in\n V. cholerae<\/jats:named-content>\n . Transcriptional activation analyses and gene silencing experiments with cells grown in sugar-supplemented M9 medium demonstrated that the ED pathway is functional in\n V. cholerae<\/jats:named-content>\n and is obligatory for gluconate catabolism. Importantly, selective activation of the ED pathway led to concurrent elevation of transcripts of prime virulence genes (\n ctxA<\/jats:italic>\n and\n tcpA<\/jats:italic>\n ) and their regulator (\n toxT<\/jats:italic>\n ). Further, lowering of these transcript levels and cholera toxin production\n in vitro<\/jats:italic>\n by an ED pathway-defective mutant (strain N16961 with a \u0394\n edd<\/jats:italic>\n mutation [\u0394\n edd<\/jats:italic>\n N16961<\/jats:sub>\n strain]) suggested the importance of this pathway in regulating\n V. cholerae<\/jats:named-content>\n virulence. The\n in vivo<\/jats:italic>\n relevance of these data was established as the mutant failed to colonize in suckling mice intestine or to induce fluid accumulation in ligated rabbit ileal loops. Activation of the ED pathway in\n V. cholerae<\/jats:named-content>\n was shown to inhibit biofilm formation\n in vitro<\/jats:italic>\n that could be reversed in the mutant. As further support for these results, comparative transcriptome analysis with cells grown in the presence of glucose or gluconate revealed that a functional ED pathway led to activation of a subset of previously reported\n in vivo<\/jats:italic>\n expressed genes. All of these results suggest the importance of the ED pathway in\n V. cholerae<\/jats:named-content>\n pathogenesis.\n <\/jats:p>","DOI":"10.1128\/jb.06379-11","type":"journal-article","created":{"date-parts":[[2012,4,29]],"date-time":"2012-04-29T00:14:06Z","timestamp":1335658446000},"page":"3377-3385","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":72,"title":["The Entner-Doudoroff Pathway Is Obligatory for Gluconate Utilization and Contributes to the Pathogenicity of Vibrio cholerae"],"prefix":"10.1128","volume":"194","author":[{"given":"Tapas","family":"Patra","sequence":"first","affiliation":[{"name":"National Institute of Cholera and Enteric Diseases, Kolkata, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hemanta","family":"Koley","sequence":"additional","affiliation":[{"name":"National Institute of Cholera and Enteric Diseases, Kolkata, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thandavarayan","family":"Ramamurthy","sequence":"additional","affiliation":[{"name":"National Institute of Cholera and Enteric Diseases, Kolkata, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Asoke C.","family":"Ghose","sequence":"additional","affiliation":[{"name":"National Institute of Cholera and Enteric Diseases, Kolkata, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ranjan K.","family":"Nandy","sequence":"additional","affiliation":[{"name":"National Institute of Cholera and Enteric Diseases, Kolkata, India"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.00279-09"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.50.3.738-744.1985"},{"key":"e_1_3_3_4_2","doi-asserted-by":"crossref","first-page":"1228","DOI":"10.1111\/j.1462-5822.2006.00703.x","article-title":"Virulence strategies for infecting phagocytes deduced from the in vivo transcriptional program of Legionella pneumophila","volume":"8","author":"Bruggemann H","year":"2006","unstructured":"BruggemannH . 2006. 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