{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,21]],"date-time":"2025-09-21T17:45:18Z","timestamp":1758476718656},"reference-count":79,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2014,4,1]],"date-time":"2014-04-01T00:00:00Z","timestamp":1396310400000},"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":[[2014,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:named-content content-type=\"genus-species\">Borrelia burgdorferi<\/jats:named-content>\n            encodes a homologue of the bacterial carbon storage regulator A (CsrA). Recently, it was reported that CsrA contributes to\n            <jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>\n            infectivity and is required for the activation of the central RpoN-RpoS regulatory pathway. However, many questions concerning the function of CsrA in\n            <jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>\n            gene regulation remain unanswered. In particular, there are conflicting reports concerning the molecular details of how CsrA may modulate\n            <jats:italic>rpoS<\/jats:italic>\n            expression and, thus, how CsrA may influence the RpoN-RpoS pathway in\n            <jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>\n            . To address these key discrepancies, we examined the role of CsrA in differential gene expression in the Lyme disease spirochete. Upon engineering an inducible\n            <jats:italic>csrA<\/jats:italic>\n            expression system in\n            <jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>\n            , controlled hyperexpression of CsrA in a merodiploid strain did not significantly alter the protein and transcript levels of\n            <jats:italic>bosR<\/jats:italic>\n            ,\n            <jats:italic>rpoS<\/jats:italic>\n            , and RpoS-dependent genes (such as\n            <jats:italic>ospC<\/jats:italic>\n            and\n            <jats:italic>dbpA<\/jats:italic>\n            ). In addition, we constructed isogenic\n            <jats:italic>csrA<\/jats:italic>\n            mutants in two widely used infectious\n            <jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>\n            strains. When expression of\n            <jats:italic>bosR<\/jats:italic>\n            ,\n            <jats:italic>rpoS<\/jats:italic>\n            ,\n            <jats:italic>ospC<\/jats:italic>\n            , and\n            <jats:italic>dbpA<\/jats:italic>\n            was compared between the\n            <jats:italic>csrA<\/jats:italic>\n            mutants and their wild-type counterparts, no detectable differences were observed. Finally, animal studies indicated that the\n            <jats:italic>csrA<\/jats:italic>\n            mutants remained infectious for and virulent in mice. Analyses of\n            <jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>\n            gene expression in mouse tissues showed comparable levels of\n            <jats:italic>rpoS<\/jats:italic>\n            transcripts by the\n            <jats:italic>csrA<\/jats:italic>\n            mutants and the parental strains. Taken together, these results constitute compelling evidence that CsrA is not involved in activation of the RpoN-RpoS pathway and is dispensable for mammalian infectious processes carried out by\n            <jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>\n            .\n          <\/jats:p>","DOI":"10.1128\/iai.01555-13","type":"journal-article","created":{"date-parts":[[2014,1,23]],"date-time":"2014-01-23T04:39:04Z","timestamp":1390451944000},"page":"1511-1522","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":15,"title":["CsrA (BB0184) Is Not Involved in Activation of the RpoN-RpoS Regulatory Pathway in Borrelia burgdorferi"],"prefix":"10.1128","volume":"82","author":[{"given":"Zhiming","family":"Ouyang","sequence":"first","affiliation":[{"name":"Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jianli","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael V.","family":"Norgard","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.7043737"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198303313081301"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.2217\/fmb.12.121"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20020770"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.72.10.5759-5767.2004"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2958.2006.05204.x"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1286-4579(03)00097-2"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro2714"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.micro.112408.134040"},{"key":"e_1_3_3_11_2","volume-title":"Borrelia: molecular biology, host interaction and pathogenesis","author":"Samuels DS","year":"2010","unstructured":"SamuelsDSRadolfJD. 2010. 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