{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T05:17:21Z","timestamp":1790745441211,"version":"4.1.0"},"reference-count":136,"publisher":"American Society for Microbiology","issue":"8","license":[{"start":{"date-parts":[[2015,8,1]],"date-time":"2015-08-01T00:00:00Z","timestamp":1438387200000},"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":[[2015,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:named-content content-type=\"genus-species\">Borrelia burgdorferi<\/jats:named-content>\n            , the Lyme disease spirochete, couples environmental sensing and gene regulation primarily via the Hk1\/Rrp1 two-component system (TCS) and Rrp2\/RpoN\/RpoS pathways. Beginning with acquisition, we reevaluated the contribution of these pathways to spirochete survival and gene regulation throughout the enzootic cycle. Live imaging of\n            <jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>\n            caught in the act of being acquired revealed that the absence of RpoS and the consequent derepression of tick-phase genes impart a Stay signal required for midgut colonization. In addition to the behavioral changes brought on by the RpoS-off state, acquisition requires activation of cyclic di-GMP (c-di-GMP) synthesis by the Hk1\/Rrp1 TCS;\n            <jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>\n            lacking either component is destroyed during the blood meal. Prior studies attributed this dramatic phenotype to a metabolic lesion stemming from reduced glycerol uptake and utilization. In a head-to-head comparison, however, the\n            <jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>\n            \u0394\n            <jats:italic>glp<\/jats:italic>\n            mutant had a markedly greater capacity to survive tick feeding than\n            <jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>\n            \u0394\n            <jats:italic>hk1<\/jats:italic>\n            or \u0394\n            <jats:italic>rrp1<\/jats:italic>\n            mutants, establishing unequivocally that glycerol metabolism is only one component of the protection afforded by c-di-GMP. Data presented herein suggest that the protective response mediated by c-di-GMP is multifactorial, involving chemotactic responses, utilization of alternate substrates for energy generation and intermediary metabolism, and remodeling of the cell envelope as a means of defending spirochetes against threats engendered during the blood meal. Expression profiling of c-di-GMP-regulated genes through the enzootic cycle supports our contention that the Hk1\/Rrp1 TCS functions primarily, if not exclusively, in ticks. These data also raise the possibility that c-di-GMP enhances the expression of a subset of RpoS-dependent genes during nymphal transmission.\n          <\/jats:p>","DOI":"10.1128\/iai.00315-15","type":"journal-article","created":{"date-parts":[[2015,5,19]],"date-time":"2015-05-19T02:11:13Z","timestamp":1432001473000},"page":"3043-3060","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":75,"title":["Cyclic di-GMP Modulates Gene Expression in Lyme Disease Spirochetes at the Tick-Mammal Interface To Promote Spirochete Survival during the Blood Meal and Tick-to-Mammal Transmission"],"prefix":"10.1128","volume":"83","author":[{"given":"Melissa J.","family":"Caimano","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Connecticut Health Center, Farmington, Connecticut, USA"},{"name":"Department of Pediatrics, University of Connecticut Health Center, Farmington, Connecticut, USA"},{"name":"Department of Molecular Biology and Biophysics, University of Connecticut Health Center, Farmington, Connecticut, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Star","family":"Dunham-Ems","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Connecticut Health Center, Farmington, Connecticut, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna M.","family":"Allard","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Connecticut Health Center, Farmington, Connecticut, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria B.","family":"Cassera","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Center for Drug Discovery, Virginia Tech, Blacksburg, Virginia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melisha","family":"Kenedy","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Oklahoma College of Medicine, Oklahoma City, Oklahoma, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Justin D.","family":"Radolf","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Connecticut Health Center, Farmington, Connecticut, USA"},{"name":"Department of Pediatrics, University of Connecticut Health Center, Farmington, Connecticut, USA"},{"name":"Department of Molecular Biology and Biophysics, University of Connecticut Health Center, Farmington, Connecticut, USA"},{"name":"Department of Genetics and Genomic Sciences, University of Connecticut Health Center, Farmington, Connecticut, USA"},{"name":"Department of Immunology, University of Connecticut Health Center, Farmington, Connecticut, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro2714"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.7043737"},{"key":"e_1_3_3_4_2","first-page":"251","volume-title":"Borrelia: molecular biology, host interaction and pathogenesis","author":"Piesman J","year":"2010","unstructured":"Piesman J, Schwan TG. 2010. 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