{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,23]],"date-time":"2025-09-23T12:50:20Z","timestamp":1758631820706},"reference-count":31,"publisher":"American Society for Microbiology","issue":"23","license":[{"start":{"date-parts":[[2004,12,1]],"date-time":"2004-12-01T00:00:00Z","timestamp":1101859200000},"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":[[2004,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:italic>Streptococcus pyogenes<\/jats:italic>\n            (the group A streptococcus [GAS]) is a medically significant pathogen of humans, causing a range of diseases from pharyngitis to necrotizing fasciitis. Several important GAS virulence genes are under the control of a pleiotropic regulator called Mga, or the multiple gene regulator of GAS, including the gene encoding the streptococcal collagen-like protein, or\n            <jats:italic>sclA<\/jats:italic>\n            . Analysis of the genome sequence upstream of\n            <jats:italic>sclA<\/jats:italic>\n            revealed two potential Mga-binding sites with homology to the published Mga-binding element, which were called P\n            <jats:italic>sclA<\/jats:italic>\n            -I (distal) and P\n            <jats:italic>sclA<\/jats:italic>\n            -II (proximal) based on their location relative to a predicted start of transcription. Primer extension was used to confirm that the Mga-dependent transcriptional start site for\n            <jats:italic>sclA<\/jats:italic>\n            was located adjacent to the proximal P\n            <jats:italic>sclA<\/jats:italic>\n            -II binding site. By using overlapping P\n            <jats:italic>sclA<\/jats:italic>\n            promoter probes and purified Mga-His fusion protein, it was shown by electrophoretic mobility shift assays that, unlike other Mga-regulated promoters, Mga binds only to a distal DNA-binding site (P\n            <jats:italic>sclA<\/jats:italic>\n            -I). Binding of Mga to P\n            <jats:italic>sclA<\/jats:italic>\n            -I could be competed with cold probes corresponding to known Mga-regulated promoters (P\n            <jats:italic>emm<\/jats:italic>\n            , P\n            <jats:italic>scpA<\/jats:italic>\n            , and P\n            <jats:italic>mga<\/jats:italic>\n            ) but not with a nonspecific probe or the proximal P\n            <jats:italic>sclA<\/jats:italic>\n            -II fragment. With the use of a plasmid-based green fluorescent protein transcriptional reporter system, the full-length P\n            <jats:italic>sclA<\/jats:italic>\n            was not sufficient to reproduce normal Mga-regulated activation. However, studies using a single-copy\n            <jats:italic>gusA<\/jats:italic>\n            transcriptional reporter system integrated at the native\n            <jats:italic>sclA<\/jats:italic>\n            chromosomal locus clearly demonstrated that the distal P\n            <jats:italic>sclA<\/jats:italic>\n            -I binding site is required for Mga regulation. Therefore, P\n            <jats:italic>sclA<\/jats:italic>\n            represents a new class of Mga-regulated promoters that requires a single distal binding site for activation.\n          <\/jats:p>","DOI":"10.1128\/jb.186.23.7847-7857.2004","type":"journal-article","created":{"date-parts":[[2004,11,16]],"date-time":"2004-11-16T23:23:00Z","timestamp":1100647380000},"page":"7847-7857","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":37,"title":["Transcriptional Activation of\n            <i>sclA<\/i>\n            by Mga Requires a Distal Binding Site in\n            <i>Streptococcus pyogenes<\/i>"],"prefix":"10.1128","volume":"186","author":[{"given":"Audry C.","family":"Almengor","sequence":"first","affiliation":[{"name":"Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kevin S.","family":"McIver","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"77","DOI":"10.1016\/0378-1119(96)00124-2","volume":"175","year":"1996","unstructured":"Andersson, G., K. 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