A RecA-LexA-dependent Pathway Mediates Ciprofloxacin-induced Fibronectin Binding in Staphylococcus aureus
Subinhibitory concentrations of ciprofloxacin (CPX) raise the fibronectin-mediated attachment of fluoroquinolone-resistant Staphylococcus aureus by selectively inducing fnbB coding for one of two fibronectin-binding proteins: FnBPB. To identify candidate regulatory pathway(s) linking drug exposure t...
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| Veröffentlicht in: | The Journal of biological chemistry 2004-03, Vol.279 (10), p.9064-9071 |
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| creator | Bisognano, Carmelo Kelley, William L. Estoppey, Tristan Francois, Patrice Schrenzel, Jacques Li, Dongmei Lew, Daniel P. Hooper, David C. Cheung, Ambrose L. Vaudaux, Pierre |
| description | Subinhibitory concentrations of ciprofloxacin (CPX) raise the fibronectin-mediated attachment of fluoroquinolone-resistant Staphylococcus aureus by selectively inducing fnbB coding for one of two fibronectin-binding proteins: FnBPB. To identify candidate regulatory pathway(s) linking drug exposure to up-regulation of fnbB, we disrupted the global response regulators agr, sarA, and recA in the highly quinolone-resistant strain RA1. Whereas agr and sarA mutants of RA1 exposed to CPX still displayed increased adhesion to fibronectin, the CPX-triggered response was abolished in the uvs-568 recA mutant, but was restored following complementation with wild type recA. Steady-state levels of recA and fnbB, but not fnbA, mRNA were co-coordinately increased >3-fold in CPX-exposed strain RA1. Electrophoretic mobility shift assays revealed specific binding of purified S. aureus SOS-repressor LexA to recA and fnbB, but not to fnbA or rpoB promoters. DNase I footprint analysis showed LexA binding overlapping the core promoter elements in fnbB. We conclude that activation of recA and derepression of lexA-regulated genes by CPX may represent a response to drug-induced damage that results in a novel induction of a virulence factor leading to increased bacterial tissue adherence. |
| doi_str_mv | 10.1074/jbc.M309836200 |
| format | Article |
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To identify candidate regulatory pathway(s) linking drug exposure to up-regulation of fnbB, we disrupted the global response regulators agr, sarA, and recA in the highly quinolone-resistant strain RA1. Whereas agr and sarA mutants of RA1 exposed to CPX still displayed increased adhesion to fibronectin, the CPX-triggered response was abolished in the uvs-568 recA mutant, but was restored following complementation with wild type recA. Steady-state levels of recA and fnbB, but not fnbA, mRNA were co-coordinately increased >3-fold in CPX-exposed strain RA1. Electrophoretic mobility shift assays revealed specific binding of purified S. aureus SOS-repressor LexA to recA and fnbB, but not to fnbA or rpoB promoters. DNase I footprint analysis showed LexA binding overlapping the core promoter elements in fnbB. We conclude that activation of recA and derepression of lexA-regulated genes by CPX may represent a response to drug-induced damage that results in a novel induction of a virulence factor leading to increased bacterial tissue adherence.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M309836200</identifier><identifier>PMID: 14699158</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>agr gene ; Anti-Infective Agents - pharmacology ; Bacterial Adhesion - drug effects ; Bacterial Proteins - metabolism ; Base Sequence ; Ciprofloxacin - pharmacology ; Fibronectins - genetics ; Fibronectins - metabolism ; Molecular Sequence Data ; Promoter Regions, Genetic ; Protein Binding ; Rec A Recombinases - genetics ; Rec A Recombinases - metabolism ; sarA gene ; Serine Endopeptidases - metabolism ; Staphylococcus aureus ; Staphylococcus aureus - metabolism</subject><ispartof>The Journal of biological chemistry, 2004-03, Vol.279 (10), p.9064-9071</ispartof><rights>2004 © 2004 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c441t-26091a5665a0839f1371337d4ebd38d98421544e059d03f37d2a7693e5cd89323</citedby><cites>FETCH-LOGICAL-c441t-26091a5665a0839f1371337d4ebd38d98421544e059d03f37d2a7693e5cd89323</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14699158$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bisognano, Carmelo</creatorcontrib><creatorcontrib>Kelley, William L.</creatorcontrib><creatorcontrib>Estoppey, Tristan</creatorcontrib><creatorcontrib>Francois, Patrice</creatorcontrib><creatorcontrib>Schrenzel, Jacques</creatorcontrib><creatorcontrib>Li, Dongmei</creatorcontrib><creatorcontrib>Lew, Daniel P.</creatorcontrib><creatorcontrib>Hooper, David C.</creatorcontrib><creatorcontrib>Cheung, Ambrose L.</creatorcontrib><creatorcontrib>Vaudaux, Pierre</creatorcontrib><title>A RecA-LexA-dependent Pathway Mediates Ciprofloxacin-induced Fibronectin Binding in Staphylococcus aureus</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Subinhibitory concentrations of ciprofloxacin (CPX) raise the fibronectin-mediated attachment of fluoroquinolone-resistant Staphylococcus aureus by selectively inducing fnbB coding for one of two fibronectin-binding proteins: FnBPB. To identify candidate regulatory pathway(s) linking drug exposure to up-regulation of fnbB, we disrupted the global response regulators agr, sarA, and recA in the highly quinolone-resistant strain RA1. Whereas agr and sarA mutants of RA1 exposed to CPX still displayed increased adhesion to fibronectin, the CPX-triggered response was abolished in the uvs-568 recA mutant, but was restored following complementation with wild type recA. Steady-state levels of recA and fnbB, but not fnbA, mRNA were co-coordinately increased >3-fold in CPX-exposed strain RA1. Electrophoretic mobility shift assays revealed specific binding of purified S. aureus SOS-repressor LexA to recA and fnbB, but not to fnbA or rpoB promoters. DNase I footprint analysis showed LexA binding overlapping the core promoter elements in fnbB. We conclude that activation of recA and derepression of lexA-regulated genes by CPX may represent a response to drug-induced damage that results in a novel induction of a virulence factor leading to increased bacterial tissue adherence.</description><subject>agr gene</subject><subject>Anti-Infective Agents - pharmacology</subject><subject>Bacterial Adhesion - drug effects</subject><subject>Bacterial Proteins - metabolism</subject><subject>Base Sequence</subject><subject>Ciprofloxacin - pharmacology</subject><subject>Fibronectins - genetics</subject><subject>Fibronectins - metabolism</subject><subject>Molecular Sequence Data</subject><subject>Promoter Regions, Genetic</subject><subject>Protein Binding</subject><subject>Rec A Recombinases - genetics</subject><subject>Rec A Recombinases - metabolism</subject><subject>sarA gene</subject><subject>Serine Endopeptidases - metabolism</subject><subject>Staphylococcus aureus</subject><subject>Staphylococcus aureus - metabolism</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc9r2zAUx8XoWLNu1x6LodCbM_2yLR3T0G6DlJZug92ELD3XKo6USnbb_PdVSKCnwXSRkD7v-56-X4ROCZ4T3PBvj62Z3zAsBaspxh_QjGDBSlaRv0dohjElpaSVOEafU3rEeXFJPqFjwmspSSVmyC2KezCLcgWvi9LCBrwFPxZ3euxf9La4Aev0CKlYuk0M3RBetXG-dN5OBmxx7doYPJjR-eIyXzr_UOTjr1Fv-u0QTDBmSoWeIkzpC_rY6SHB18N-gv5cX_1e_ihXt99_Lher0nBOxpLWWBJd1XWl809kR1hDGGssh9YyYaXglFScA66kxazLL1Q3tWRQGSsko-wEXex188BPE6RRrV0yMAzaQ5iSakiThf8DJJLWTDCewfkeNDGkFKFTm-jWOm4VwWqXgsopqPcUcsHZQXlq12Df8YPtGTjfA7176F9cBNW6YHpYK9rInarE9a6v2FOQ7Xp2EFUyDnw2PleYUdng_jXBGyqZoH4</recordid><startdate>20040305</startdate><enddate>20040305</enddate><creator>Bisognano, Carmelo</creator><creator>Kelley, William L.</creator><creator>Estoppey, Tristan</creator><creator>Francois, Patrice</creator><creator>Schrenzel, Jacques</creator><creator>Li, Dongmei</creator><creator>Lew, Daniel P.</creator><creator>Hooper, David C.</creator><creator>Cheung, Ambrose L.</creator><creator>Vaudaux, Pierre</creator><general>Elsevier Inc</general><general>American Society for Biochemistry and Molecular Biology</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7TM</scope><scope>C1K</scope><scope>7X8</scope></search><sort><creationdate>20040305</creationdate><title>A RecA-LexA-dependent Pathway Mediates Ciprofloxacin-induced Fibronectin Binding in Staphylococcus aureus</title><author>Bisognano, Carmelo ; Kelley, William L. ; Estoppey, Tristan ; Francois, Patrice ; Schrenzel, Jacques ; Li, Dongmei ; Lew, Daniel P. ; Hooper, David C. ; Cheung, Ambrose L. ; Vaudaux, Pierre</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c441t-26091a5665a0839f1371337d4ebd38d98421544e059d03f37d2a7693e5cd89323</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>agr gene</topic><topic>Anti-Infective Agents - pharmacology</topic><topic>Bacterial Adhesion - drug effects</topic><topic>Bacterial Proteins - metabolism</topic><topic>Base Sequence</topic><topic>Ciprofloxacin - pharmacology</topic><topic>Fibronectins - genetics</topic><topic>Fibronectins - metabolism</topic><topic>Molecular Sequence Data</topic><topic>Promoter Regions, Genetic</topic><topic>Protein Binding</topic><topic>Rec A Recombinases - genetics</topic><topic>Rec A Recombinases - metabolism</topic><topic>sarA gene</topic><topic>Serine Endopeptidases - metabolism</topic><topic>Staphylococcus aureus</topic><topic>Staphylococcus aureus - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bisognano, Carmelo</creatorcontrib><creatorcontrib>Kelley, William L.</creatorcontrib><creatorcontrib>Estoppey, Tristan</creatorcontrib><creatorcontrib>Francois, Patrice</creatorcontrib><creatorcontrib>Schrenzel, Jacques</creatorcontrib><creatorcontrib>Li, Dongmei</creatorcontrib><creatorcontrib>Lew, Daniel P.</creatorcontrib><creatorcontrib>Hooper, David C.</creatorcontrib><creatorcontrib>Cheung, Ambrose L.</creatorcontrib><creatorcontrib>Vaudaux, Pierre</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Nucleic Acids Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bisognano, Carmelo</au><au>Kelley, William L.</au><au>Estoppey, Tristan</au><au>Francois, Patrice</au><au>Schrenzel, Jacques</au><au>Li, Dongmei</au><au>Lew, Daniel P.</au><au>Hooper, David C.</au><au>Cheung, Ambrose L.</au><au>Vaudaux, Pierre</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A RecA-LexA-dependent Pathway Mediates Ciprofloxacin-induced Fibronectin Binding in Staphylococcus aureus</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>2004-03-05</date><risdate>2004</risdate><volume>279</volume><issue>10</issue><spage>9064</spage><epage>9071</epage><pages>9064-9071</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><abstract>Subinhibitory concentrations of ciprofloxacin (CPX) raise the fibronectin-mediated attachment of fluoroquinolone-resistant Staphylococcus aureus by selectively inducing fnbB coding for one of two fibronectin-binding proteins: FnBPB. To identify candidate regulatory pathway(s) linking drug exposure to up-regulation of fnbB, we disrupted the global response regulators agr, sarA, and recA in the highly quinolone-resistant strain RA1. Whereas agr and sarA mutants of RA1 exposed to CPX still displayed increased adhesion to fibronectin, the CPX-triggered response was abolished in the uvs-568 recA mutant, but was restored following complementation with wild type recA. Steady-state levels of recA and fnbB, but not fnbA, mRNA were co-coordinately increased >3-fold in CPX-exposed strain RA1. Electrophoretic mobility shift assays revealed specific binding of purified S. aureus SOS-repressor LexA to recA and fnbB, but not to fnbA or rpoB promoters. DNase I footprint analysis showed LexA binding overlapping the core promoter elements in fnbB. 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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | agr gene Anti-Infective Agents - pharmacology Bacterial Adhesion - drug effects Bacterial Proteins - metabolism Base Sequence Ciprofloxacin - pharmacology Fibronectins - genetics Fibronectins - metabolism Molecular Sequence Data Promoter Regions, Genetic Protein Binding Rec A Recombinases - genetics Rec A Recombinases - metabolism sarA gene Serine Endopeptidases - metabolism Staphylococcus aureus Staphylococcus aureus - metabolism |
| title | A RecA-LexA-dependent Pathway Mediates Ciprofloxacin-induced Fibronectin Binding in Staphylococcus aureus |
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