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Expression of the toxin genes\n            <jats:italic>pagA<\/jats:italic>\n            ,\n            <jats:italic>lef<\/jats:italic>\n            , and\n            <jats:italic>cya<\/jats:italic>\n            peaks in late log phase, and steady-state levels of the toxin proteins are highest during the transition into stationary phase. Here we show that an apparent transition state regulator negatively regulates toxin gene expression. We identified two orthologues of the\n            <jats:italic>B. subtilis<\/jats:italic>\n            transition state regulator\n            <jats:italic>abrB<\/jats:italic>\n            in the\n            <jats:italic>B. anthracis<\/jats:italic>\n            genome: one on the chromosome and one on the 182-kb virulence plasmid pXO1. The orthologue located on the chromosome is predicted to encode a 94-amino-acid protein that is 85% identical to\n            <jats:italic>B. subtilis<\/jats:italic>\n            AbrB. The hypothetical protein encoded on pXO1 is 41% identical to\n            <jats:italic>B. subtilis<\/jats:italic>\n            AbrB but missing 27 amino acid residues from the amino terminus compared to the\n            <jats:italic>B. subtilis<\/jats:italic>\n            protein. Deletion of the pXO1-encoded\n            <jats:italic>abrB<\/jats:italic>\n            orthologue did not affect toxin gene expression under the conditions tested. However, a\n            <jats:italic>B. anthracis<\/jats:italic>\n            mutant in which the chromosomal\n            <jats:italic>abrB<\/jats:italic>\n            gene was deleted expressed\n            <jats:italic>pagA<\/jats:italic>\n            earlier and at a higher level than the parent strain. Expression of a transcriptional\n            <jats:italic>pagA-lacZ<\/jats:italic>\n            fusion in the\n            <jats:italic>abrB<\/jats:italic>\n            mutant was increased up to 20-fold during early exponential growth compared to the parent strain and peaked in mid-exponential rather than late exponential phase. In contrast to the strong effect of\n            <jats:italic>abrB<\/jats:italic>\n            on\n            <jats:italic>pagA<\/jats:italic>\n            expression,\n            <jats:italic>lef-lacZ<\/jats:italic>\n            and\n            <jats:italic>cya-lacZ<\/jats:italic>\n            expression during early-log-phase growth was increased only two- to threefold in the\n            <jats:italic>abrB<\/jats:italic>\n            null mutant. Western hybridization analysis showed increased PA, LF, and EF synthesis by the mutant. As is true in\n            <jats:italic>B. subtilis<\/jats:italic>\n            , the\n            <jats:italic>B. anthracis abrB<\/jats:italic>\n            gene is negatively regulated by\n            <jats:italic>spo0A<\/jats:italic>\n            . Our findings tie anthrax toxin gene expression to the complex network of postexponential phase adaptive responses that have been well studied in\n            <jats:italic>B. subtilis<\/jats:italic>\n            .\n          <\/jats:p>","DOI":"10.1128\/jb.184.2.370-380.2002","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T10:01:09Z","timestamp":1027764069000},"page":"370-380","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":127,"title":["Control of Anthrax Toxin Gene Expression by the Transition State Regulator\n            <i>abrB<\/i>"],"prefix":"10.1128","volume":"184","author":[{"given":"Elke","family":"Saile","sequence":"first","affiliation":[{"name":"Department of Microbiology and Molecular Genetics, The University of Texas-Houston Health Science Center Medical School, Houston, Texas 77030"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Theresa M.","family":"Koehler","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Molecular Genetics, The University of Texas-Houston Health Science Center Medical School, Houston, Texas 77030"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"97","DOI":"10.1111\/j.1365-2958.1994.tb00405.x","volume":"13","year":"1994","unstructured":"Agaisse, H., and D. 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