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Microarray analysis of mutants lacking the\n            <jats:underline>\n              <jats:italic>B<\/jats:italic>\n            <\/jats:underline>\n            <jats:italic>orrelia<\/jats:italic>\n            host\n            <jats:underline>ad<\/jats:underline>\n            aptation\n            <jats:underline>r<\/jats:underline>\n            egulator (BadR) revealed the downregulation of genes encoding enzymes whose role in the pathophysiology of\n            <jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>\n            is unknown. Immunoblot analysis of the\n            <jats:italic>badR<\/jats:italic>\n            mutants confirmed reduced levels of these enzymes, and one of these enzymes, encoded by\n            <jats:italic>bb0086<\/jats:italic>\n            , shares homology to prokaryotic magnesium chelatase and Lon-type proteases. The BB0086 levels in\n            <jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>\n            were higher under conditions mimicking those in fed ticks. Mutants lacking\n            <jats:italic>bb0086<\/jats:italic>\n            had no apparent\n            <jats:italic>in vitro<\/jats:italic>\n            growth defect but were incapable of colonizing immunocompetent C3H\/HeN or immunodeficient SCID mice. Immunoblot analysis revealed reduced levels of proteins critical for the adaptation of\n            <jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>\n            to the mammalian host, such as OspC, DbpA, and BBK32. Both RpoS and BosR, key regulators of gene expression in\n            <jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>\n            , were downregulated in the\n            <jats:italic>bb0086<\/jats:italic>\n            mutants. Therefore, we designated BB0086 the\n            <jats:underline>\n              <jats:italic>B<\/jats:italic>\n            <\/jats:underline>\n            <jats:italic>orrelia<\/jats:italic>\n            host\n            <jats:underline>ad<\/jats:underline>\n            aptation\n            <jats:underline>p<\/jats:underline>\n            rotein (BadP). Unlike\n            <jats:italic>badP<\/jats:italic>\n            mutants, the control strains established infection in C3H\/HeN mice at 4 days postinfection, indicating an early colonization defect in mutants due to reduced levels of the lipoproteins\/regulators critical for initial stages of infection. However,\n            <jats:italic>badP<\/jats:italic>\n            mutants survived within dialysis membrane chambers (DMCs) implanted within the rat peritoneal cavity but, unlike the control strains, did not display complete switching of OspA to OspC, suggesting incomplete adaptation to the mammalian phase of infection. These findings have opened a novel regulatory mechanism which impacts the virulence potential of\n            <jats:italic>B<\/jats:italic>\n            .\n            <jats:named-content content-type=\"genus-species\">burgdorferi<\/jats:named-content>\n            .\n          <\/jats:p>","DOI":"10.1128\/iai.00057-18","type":"journal-article","created":{"date-parts":[[2018,4,20]],"date-time":"2018-04-20T10:33:53Z","timestamp":1524220433000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":10,"title":["Borrelia Host Adaptation Protein (BadP) Is Required for the Colonization of a Mammalian Host by the Agent of Lyme Disease"],"prefix":"10.1128","volume":"86","author":[{"suffix":"II","given":"Trever C.","family":"Smith","sequence":"first","affiliation":[{"name":"South Texas Center for Emerging Infectious Diseases (STCEID), Center of Excellence in Infection Genomics and Department of Biology, The University of Texas at San Antonio, San Antonio, Texas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah M.","family":"Helm","sequence":"additional","affiliation":[{"name":"South Texas Center for Emerging Infectious Diseases (STCEID), Center of Excellence in Infection Genomics and Department of Biology, The University of Texas at San Antonio, San Antonio, Texas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yue","family":"Chen","sequence":"additional","affiliation":[{"name":"South Texas Center for Emerging Infectious Diseases (STCEID), Center of Excellence in Infection Genomics and Department of Biology, The University of Texas at San Antonio, San Antonio, Texas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ying-Han","family":"Lin","sequence":"additional","affiliation":[{"name":"South Texas Center for Emerging Infectious Diseases (STCEID), Center of Excellence in Infection Genomics and Department of Biology, The University of Texas at San Antonio, San Antonio, Texas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S. L.","family":"Rajasekhar Karna","sequence":"additional","affiliation":[{"name":"South Texas Center for Emerging Infectious Diseases (STCEID), Center of Excellence in Infection Genomics and Department of Biology, The University of Texas at San Antonio, San Antonio, Texas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Seshu","sequence":"additional","affiliation":[{"name":"South Texas Center for Emerging Infectious Diseases (STCEID), Center of Excellence in Infection Genomics and Department of Biology, The University of Texas at San Antonio, San Antonio, Texas, 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