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The oxygen-sensing transcription factor, FNR, is essential for transcription activation at the\n                      <jats:italic>aniA<\/jats:italic>\n                      promoter, and full activation also requires the two-component regulatory system, NarQ-NarP, and the presence of nitrite. The only other gene known to be activated by the gonococcal FNR is\n                      <jats:italic>ccp<\/jats:italic>\n                      encoding a cytochrome\n                      <jats:italic>c<\/jats:italic>\n                      peroxidase, and no FNR-repressed genes have been reported in the gonococcus. In contrast, FNR acts as both an activator and repressor involved in the control of more than 100 operons in\n                      <jats:italic>E. coli<\/jats:italic>\n                      regulating major changes in the adaptation from aerobic to anaerobic conditions. In this study we have performed a microarray-led investigation of the FNR-mediated responses in\n                      <jats:italic>N. gonorrhoeae<\/jats:italic>\n                      to determine the physiological similarities and differences in the role of FNR in cellular regulation in this species.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Microarray experiments show that\n                      <jats:italic>N. gonorrhoeae<\/jats:italic>\n                      FNR controls a much smaller regulon than its\n                      <jats:italic>E. coli<\/jats:italic>\n                      counterpart; it activates transcription of\n                      <jats:italic>aniA<\/jats:italic>\n                      and thirteen other genes, and represses transcription of six genes that include\n                      <jats:italic>dnrN<\/jats:italic>\n                      and\n                      <jats:italic>norB<\/jats:italic>\n                      . Having previously shown that a single amino acid substitution is sufficient to enable the gonococcal FNR to complement an\n                      <jats:italic>E. coli fnr<\/jats:italic>\n                      mutation, we investigated whether the gonococcal NarQ-NarP can substitute for\n                      <jats:italic>E. coli<\/jats:italic>\n                      NarX-NarL or NarQ-NarP. A plasmid expressing gonococcal\n                      <jats:italic>narQ-narP<\/jats:italic>\n                      was unable to complement\n                      <jats:italic>E. coli narQP<\/jats:italic>\n                      or\n                      <jats:italic>narXL<\/jats:italic>\n                      mutants, and was insensitive to nitrate or nitrite. Mutations that progressively changed the periplasmic nitrate sensing region, the P box, of\n                      <jats:italic>E. coli<\/jats:italic>\n                      NarQ to the sequence of the corresponding region of gonococcal NarQ resulted in loss of transcription activation in response to the availability of either nitrate or nitrite. However, the previously reported ligand-insensitive ability of gonococcal NarQ, the \"locked on\" phenotype, to activate either\n                      <jats:italic>E. coli<\/jats:italic>\n                      NarL or NarP was confirmed.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Despite the sequence similarities between transcription activators of\n                      <jats:italic>E. coli<\/jats:italic>\n                      and\n                      <jats:italic>N. gonorrhoeae<\/jats:italic>\n                      , these results emphasise the fundamental differences in transcription regulation between these two types of pathogenic bacteria.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/1471-2164-8-35","type":"journal-article","created":{"date-parts":[[2007,2,21]],"date-time":"2007-02-21T14:26:22Z","timestamp":1172067982000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":43,"title":["The small FNR regulon of Neisseria gonorrhoeae: comparison with the larger Escherichia coli FNR regulon and interaction with the NarQ-NarP regulon"],"prefix":"10.1186","volume":"8","author":[{"given":"Rebekah N","family":"Whitehead","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tim W","family":"Overton","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lori AS","family":"Snyder","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simon J","family":"McGowan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harry","family":"Smith","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeff A","family":"Cole","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nigel J","family":"Saunders","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2007,1,29]]},"reference":[{"key":"748_CR1","doi-asserted-by":"publisher","first-page":"86","DOI":"10.1093\/clinids\/8.1.86","volume":"8","author":"TG Burnakis","year":"1986","unstructured":"Burnakis TG, Hildebrandt NB: Pelvic inflammatory disease: a review with emphasis on antimicrobial therapy. 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