{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T17:14:18Z","timestamp":1777655658043,"version":"3.51.4"},"reference-count":62,"publisher":"American Society for Microbiology","issue":"15","license":[{"start":{"date-parts":[[2013,8,1]],"date-time":"2013-08-01T00:00:00Z","timestamp":1375315200000},"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":[[2013,8]]},"abstract":"ABSTRACT<\/jats:title>\n \n The enzyme cofactor biotin (vitamin H or B7) is an energetically expensive molecule whose\n de novo<\/jats:italic>\n biosynthesis requires 20 ATP equivalents. It seems quite likely that diverse mechanisms have evolved to tightly regulate its biosynthesis. Unlike the model regulator BirA, a bifunctional biotin protein ligase with the capability of repressing the biotin biosynthetic pathway, BioR has been recently reported by us as an alternative machinery and a new type of GntR family transcriptional factor that can repress the expression of the\n bioBFDAZ<\/jats:italic>\n operon in the plant pathogen\n Agrobacterium tumefaciens<\/jats:named-content>\n . However, quite unusually, a closely related human pathogen,\n Brucella melitensis<\/jats:named-content>\n , has four putative BioR-binding sites (both\n bioR<\/jats:italic>\n and\n bioY<\/jats:italic>\n possess one site in the promoter region, whereas the\n bioBFDAZ<\/jats:italic>\n [\n bio<\/jats:italic>\n ] operon contains two tandem BioR boxes). This raised the question of whether BioR mediates the complex regulatory network of biotin metabolism. Here, we report that this is the case. The\n B. melitensis<\/jats:named-content>\n BioR ortholog was overexpressed and purified to homogeneity, and its solution structure was found to be dimeric. Functional complementation in a\n bioR<\/jats:italic>\n isogenic mutant of\n A. tumefaciens<\/jats:named-content>\n elucidated that\n Brucella<\/jats:named-content>\n BioR is a functional repressor. Electrophoretic mobility shift assays demonstrated that the four predicted BioR sites of\n Brucella<\/jats:named-content>\n plus the BioR site of\n A. tumefaciens<\/jats:named-content>\n can all interact with the\n Brucella<\/jats:named-content>\n BioR protein. In a reporter strain that we developed on the basis of a double mutant of\n A. tumefaciens<\/jats:named-content>\n (the \u0394\n bioR<\/jats:italic>\n \u0394\n bioBFDA<\/jats:italic>\n mutant), the \u03b2-galactosidase (\u03b2-Gal) activity of three plasmid-borne transcriptional fusions (\n bioB<\/jats:italic>\n bme\n -lacZ<\/jats:italic>\n ,\n bioY<\/jats:italic>\n bme\n -lacZ<\/jats:italic>\n , and\n bioR<\/jats:italic>\n bme\n -lacZ<\/jats:italic>\n ) was dramatically decreased upon overexpression of\n Brucella bioR<\/jats:named-content>\n . Real-time quantitative PCR analyses showed that the expression of\n bioBFDA<\/jats:italic>\n and\n bioY<\/jats:italic>\n is significantly elevated upon removal of\n bioR<\/jats:italic>\n from\n B. melitensis<\/jats:named-content>\n . Together, we conclude that\n Brucella<\/jats:named-content>\n BioR is not only a negative autoregulator but also a repressor of expression of\n bioY<\/jats:italic>\n and\n bio<\/jats:italic>\n operons that separately function in biotin transport and the biosynthesis pathway.\n <\/jats:p>","DOI":"10.1128\/jb.00378-13","type":"journal-article","created":{"date-parts":[[2013,6,1]],"date-time":"2013-06-01T05:58:20Z","timestamp":1370066300000},"page":"3451-3467","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":29,"title":["Brucella BioR Regulator Defines a Complex Regulatory Mechanism for Bacterial Biotin Metabolism"],"prefix":"10.1128","volume":"195","author":[{"given":"Youjun","family":"Feng","sequence":"first","affiliation":[{"name":"Department of Microbiology, University of Illinois, Urbana, Illinois, USA"},{"name":"Institute of Microbiology, College of Life Science, Zhejiang University, Hangzhou, Zhejiang, People's Republic of China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jie","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Infectious Disease Control, Beijing Institute of Disease Control and Prevention, Beijing, People's Republic of China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Huimin","family":"Zhang","sequence":"additional","affiliation":[{"name":"Institute for Genomic Biology, University of Illinois, Urbana, Illinois, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zeliang","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Infectious Disease Control, Beijing Institute of Disease Control and Prevention, Beijing, People's Republic of China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Swaminath","family":"Srinivas","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, University of Illinois, Urbana, Illinois, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"443","DOI":"10.1146\/annurev.genet.41.042007.170450","article-title":"Biotin sensing: universal influence of biotin status on transcription","volume":"41","author":"Beckett D","year":"2007","unstructured":"BeckettD. 2007. 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