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Here we report that the ability to produce a normal foregut-blocking infection depends on induction of the<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Y. pestis<\/jats:named-content>PhoP-PhoQ two-component regulatory system in the flea.<jats:italic>Y. pestis phoP<\/jats:italic>-negative mutants achieved normal infection rates and bacterial loads in the flea midgut but produced a less cohesive biofilm both<jats:italic>in vitro<\/jats:italic>and in the flea and had a greatly reduced ability to localize to and block the flea foregut. Thus, not only is the PhoP-PhoQ system induced in the flea gut environment, but also this induction is required to produce a normal transmissible infection. The altered biofilm phenotype in the flea was not due to lack of PhoPQ-dependent or PmrAB-dependent addition of aminoarabinose to the<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Y. pestis<\/jats:named-content>lipid A, because an aminoarabinose-deficient mutant that is highly sensitive to cationic antimicrobial peptides had a normal phenotype in the flea digestive tract. In addition to enhancing transmissibility, induction of the PhoP-PhoQ system in the arthropod vector prior to transmission may preadapt<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Y. pestis<\/jats:named-content>to resist the initial encounter with the mammalian innate immune response.<\/jats:p>","DOI":"10.1128\/jb.02000-12","type":"journal-article","created":{"date-parts":[[2013,2,23]],"date-time":"2013-02-23T11:58:53Z","timestamp":1361620733000},"page":"1920-1930","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":64,"title":["Induction of the Yersinia pestis PhoP-PhoQ Regulatory System in the Flea and Its Role in Producing a Transmissible Infection"],"prefix":"10.1128","volume":"195","author":[{"given":"Roberto","family":"Rebeil","sequence":"first","affiliation":[{"name":"Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Clayton O.","family":"Jarrett","sequence":"additional","affiliation":[{"name":"Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James D.","family":"Driver","sequence":"additional","affiliation":[{"name":"Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert K.","family":"Ernst","sequence":"additional","affiliation":[{"name":"Departments of Microbiology and Medicine, University of Washington, Seattle, Washington, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Petra C. 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