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In humans,<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">H. ducreyi<\/jats:named-content>is surrounded by phagocytes and must adapt to a hostile environment to survive. To sense and respond to environmental cues, bacteria frequently use two-component signal transduction (2CST) systems. The only obvious 2CST system in<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">H. ducreyi<\/jats:named-content>is CpxRA; CpxR is a response regulator, and CpxA is a sensor kinase. Previous studies by Hansen and coworkers showed that CpxR directly represses the expression of<jats:italic>dsrA<\/jats:italic>, the<jats:italic>lspB<\/jats:italic>-<jats:italic>lspA2<\/jats:italic>operon, and the<jats:italic>flp<\/jats:italic>operon, which are required for virulence in humans. They further showed that CpxA functions predominantly as a phosphatase<jats:italic>in vitro<\/jats:italic>to maintain the expression of virulence determinants. Since a<jats:italic>cpxA<\/jats:italic>mutant is avirulent while a<jats:italic>cpxR<\/jats:italic>mutant is fully virulent in humans, CpxA also likely functions predominantly as a phosphatase<jats:italic>in vivo<\/jats:italic>. To better understand the role of<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">H. ducreyi<\/jats:named-content>CpxRA in controlling virulence determinants, here we defined genes potentially regulated by CpxRA by using RNA-Seq. Activation of CpxR by deletion of<jats:italic>cpxA<\/jats:italic>repressed nearly 70% of its targets, including seven established virulence determinants. Inactivation of CpxR by deletion of<jats:italic>cpxR<\/jats:italic>differentially regulated few genes and increased the expression of one virulence determinant. We identified a CpxR binding motif that was enriched in downregulated but not upregulated targets. These data reinforce the hypothesis that CpxA phosphatase activity plays a critical role in controlling<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">H. ducreyi<\/jats:named-content>virulence<jats:italic>in vivo<\/jats:italic>. Characterization of the downregulated genes may offer new insights into pathogenesis.<\/jats:p>","DOI":"10.1128\/jb.00372-13","type":"journal-article","created":{"date-parts":[[2013,6,1]],"date-time":"2013-06-01T05:58:20Z","timestamp":1370066300000},"page":"3486-3502","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":36,"title":["Activation of CpxRA in Haemophilus ducreyi Primarily Inhibits the Expression of Its Targets, Including Major Virulence Determinants"],"prefix":"10.1128","volume":"195","author":[{"given":"Dharanesh","family":"Gangaiah","sequence":"first","affiliation":[{"name":"Departments of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xinjun","family":"Zhang","sequence":"additional","affiliation":[{"name":"Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, Indiana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kate R.","family":"Fortney","sequence":"additional","affiliation":[{"name":"Departments of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Beth","family":"Baker","sequence":"additional","affiliation":[{"name":"Center for Microbial Pathogenesis, Nationwide Children's Hospital, Columbus, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yunlong","family":"Liu","sequence":"additional","affiliation":[{"name":"Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, Indiana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr","given":"Robert S.","family":"Munson","sequence":"additional","affiliation":[{"name":"Center for Microbial Pathogenesis, Nationwide Children's Hospital, Columbus, Ohio, USA"},{"name":"Department of Pediatrics, The Ohio State University College of Medicine, Columbus, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stanley M.","family":"Spinola","sequence":"additional","affiliation":[{"name":"Departments of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA"},{"name":"Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA"},{"name":"Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA"},{"name":"Center for Immunobiology, Indiana University School of Medicine, Indianapolis, Indiana, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","first-page":"818","article-title":"Eradicating chancroid","volume":"79","author":"Steen R","year":"2001","unstructured":"SteenR. 2001. 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