{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T14:16:01Z","timestamp":1790691361753,"version":"4.1.0"},"reference-count":35,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2009,1,1]],"date-time":"2009-01-01T00:00:00Z","timestamp":1230768000000},"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":["J Bacteriol"],"published-print":{"date-parts":[[2009,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The MtrR transcriptional-regulatory protein is known to repress transcription of the\n            <jats:italic>mtrCDE<\/jats:italic>\n            operon, which encodes a multidrug efflux pump possessed by\n            <jats:italic>Neisseria gonorrhoeae<\/jats:italic>\n            that is important in the ability of gonococci to resist certain hydrophobic antibiotics, detergents, dyes, and host-derived antimicrobials. In order to determine whether MtrR can exert regulatory action on other gonococcal genes, we performed a whole-genome microarray analysis using total RNA extracted from actively growing broth cultures of isogenic MtrR-positive and MtrR-negative gonococci. We determined that, at a minimum, 69 genes are directly or indirectly subject to MtrR control, with 47 being MtrR repressed and 22 being MtrR activated.\n            <jats:italic>rpoH<\/jats:italic>\n            , which encodes the general stress response sigma factor RpoH (sigma 32), was found by DNA-binding studies to be directly repressed by MtrR, as it was found to bind to a DNA sequence upstream of\n            <jats:italic>rpoH<\/jats:italic>\n            that included sites within the\n            <jats:italic>rpoH<\/jats:italic>\n            promoter. MtrR also repressed the expression of certain RpoH-regulated genes, but this regulation was likely indirect and a reflection of MtrR control of\n            <jats:italic>rpoH<\/jats:italic>\n            expression. Inducible expression of MtrR was found to repress\n            <jats:italic>rpoH<\/jats:italic>\n            expression and to increase gonococcal susceptibility to hydrogen peroxide (H\n            <jats:sub>2<\/jats:sub>\n            O\n            <jats:sub>2<\/jats:sub>\n            ) and an antibiotic (erythromycin) recognized by the MtrC-MtrD-MtrE efflux pump system. We propose that, apart from its ability to control the expression of the\n            <jats:italic>mtrCDE<\/jats:italic>\n            -encoded efflux pump operon and, as a consequence, levels of gonococcal resistance to host antimicrobials (e.g., antimicrobial peptides) recognized by the efflux pump, the ability of MtrR to regulate the expression levels of\n            <jats:italic>rpoH<\/jats:italic>\n            and RpoH-regulated genes also modulates levels of gonococcal susceptibility to H\n            <jats:sub>2<\/jats:sub>\n            O\n            <jats:sub>2<\/jats:sub>\n            .\n          <\/jats:p>","DOI":"10.1128\/jb.01165-08","type":"journal-article","created":{"date-parts":[[2008,11,1]],"date-time":"2008-11-01T00:55:26Z","timestamp":1225500926000},"page":"287-297","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":57,"title":["MtrR Modulates\n            <i>rpoH<\/i>\n            Expression and Levels of Antimicrobial Resistance in\n            <i>Neisseria gonorrhoeae<\/i>"],"prefix":"10.1128","volume":"191","author":[{"given":"Jason P.","family":"Folster","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia 30322"},{"name":"Laboratories of Bacterial Pathogenesis, VA Medical Center, Decatur, Georgia 30033"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul J. T.","family":"Johnson","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia 30322"},{"name":"Laboratories of Bacterial Pathogenesis, VA Medical Center, Decatur, Georgia 30033"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lydgia","family":"Jackson","sequence":"additional","affiliation":[{"name":"Laboratory for Genomics and Bioinformatics"},{"name":"Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vijaya","family":"Dhulipali","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia 30322"},{"name":"Laboratories of Bacterial Pathogenesis, VA Medical Center, Decatur, Georgia 30033"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David W.","family":"Dyer","sequence":"additional","affiliation":[{"name":"Laboratory for Genomics and Bioinformatics"},{"name":"Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William M.","family":"Shafer","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia 30322"},{"name":"Laboratories of Bacterial Pathogenesis, VA Medical Center, Decatur, Georgia 30033"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/JB.00644-06"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.74.5.2767-2776.2006"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.73.8.4834-4845.2005"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/JB.187.14.4865-4874.2005"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/JB.187.11.3713-3720.2005"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/JB.00286-07"},{"key":"e_1_3_2_8_2","first-page":"S12","volume":"74","year":"1998","unstructured":"Gerbase, A. C., J. T. Rowley, D. H. Heymann, S. F. Berkley, and P. Piot. 1998. Global prevalence and incidence estimates of selected curable STDs. Sex. Transm. Infect. 74(Suppl.):S12-S16.","journal-title":"Sex. Transm. Infect."},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1128\/JB.01807-05"},{"key":"e_1_3_2_10_2","first-page":"509","volume":"251","year":"1996","unstructured":"Gunn, J. S., and D. C. Stein. 1996. Use of a non-selective transformation technique to construct a multiply restriction\/modification-deficient mutant of Neisseria gonorrhoeae. Mol. Gen. Genet. 251 : 509-517.","journal-title":"Mol. Gen. Genet."},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1128\/jb.177.14.4162-4165.1995"},{"key":"e_1_3_2_12_2","doi-asserted-by":"crossref","first-page":"2117","DOI":"10.1099\/00221287-143-7-2117","volume":"143","year":"1997","unstructured":"Hagman, K. E., C. E. Lucas, J. T. Balthazar, L. Snyder, M. Nilles, R. C. Judd, and W. M. Shafer. 1997. 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Induction of the mtrCDE-encoded efflux pump system of Neisseria gonorrhoeae requires MtrA, an AraC-like protein. Mol. Microbiol. 33 : 651-658.","journal-title":"Mol. Microbiol."},{"key":"e_1_3_2_22_2","first-page":"187","year":"2001","unstructured":"Rouquette-Loughlin, C., W. L. Veal, E.-H. Lee, L. Zarantonelli, J. T. Balthazar, and W. M. Shafer. 2001. Antimicrobial efflux systems possessed by Neisseria gonorrhoeae and Neisseria meningitidis viewed as virulence factors, p. 187-200. In I. T. Paulsen and K. Lewis (ed.), Multidrug efflux. Horizon Scientific Press, Wymonham, United Kingdom.","journal-title":"Multidrug efflux."},{"key":"e_1_3_2_23_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.25.6.767"},{"key":"e_1_3_2_24_2","doi-asserted-by":"crossref","first-page":"907","DOI":"10.1099\/13500872-141-4-907","volume":"141","year":"1995","unstructured":"Shafer, W. M., J. T. Balthazar, K. E. Hagman, and S. A. Morse. 1995. 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