Identification and Characterization of alcR, a Gene Encoding an AraC-Like Regulator of Alcaligin Siderophore Biosynthesis and Transport in Bordetella pertussis and Bordetella bronchiseptica

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dc.contributor.authorBeaumont, Fiona C.en_US
dc.contributor.authorKang, Ho Youngen_US
dc.contributor.authorBrickman, Timothy J.en_US
dc.contributor.authorArmstrong, Sandra K.en_US
dc.date.accessioned2011-04-29T13:16:14Zen_US
dc.date.accessioned2011-05-17T01:40:07Z
dc.date.available2011-04-29T13:16:14Zen_US
dc.date.available2011-05-17T01:40:07Z
dc.date.issued1998-02en_US
dc.description.abstractA Bordetella bronchiseptica iron transport mutant was isolated following an enrichment procedure based on streptonigrin resistance. The mutant displayed a growth defect on iron-restricted medium containing ferric alcaligin as the sole iron source. In addition to the apparent inability to acquire iron from the siderophore, the mutant failed to produce alcaligin as well as two known iron-regulated proteins, one of which is the AlcC alcaligin biosynthesis protein. A 1.6-kb KpnI-PstI Bordetella pertussis DNA fragment mapping downstream of the alcaligin biosynthesis genes alcABC restored both siderophore biosynthesis and expression of the ironregulated proteins to the mutant. Nucleotide sequencing of this complementing 1.6-kb region identified an open reading frame predicted to encode a protein with strong similarity to members of the AraC family of transcriptional regulators, for which we propose the gene designation alcR. Primer extension analysis localized an iron-regulated transcription initiation site upstream of the alcR open reading frame and adjacent to sequences homologous to the consensus Fur repressor binding site. The AlcR protein was produced by using an Escherichia coli expression system and visualized in electrophoretic gels. In-frame alcR deletion mutants of B. pertussis and B. bronchiseptica were constructed, and the defined mutants exhibited the alcR mutant phenotype, characterized by the inability to produce and transport alcaligin and express the two iron-repressed proteins. The cloned alcR gene provided in trans restored these siderophore system activities to the mutants. Together, these results indicate that AlcR is involved in the regulation of Bordetella alcaligin biosynthesis and transport genes and is required for their full expression. Originally published Journal of Bacteriology, Vol. 180, No. 4, Feb 1998en_US
dc.identifier.citationJournal of Bacteriology; 180:4 p. 862-870en_US
dc.identifier.pmidPMC106965en_US
dc.identifier.urihttp://hdl.handle.net/10342/3448en_US
dc.language.isoen_USen_US
dc.publisherEast Carolina Universityen_US
dc.relation.urihttp://jb.asm.org/archive/1998.dtlen_US
dc.rightsAuthor notified of opt-out rights by Cammie Jennings prior to upload of this article.en_US
dc.subjectBordetella bronchisepticaen_US
dc.subjectSiderophoreen_US
dc.subjectAlcaliginen_US
dc.titleIdentification and Characterization of alcR, a Gene Encoding an AraC-Like Regulator of Alcaligin Siderophore Biosynthesis and Transport in Bordetella pertussis and Bordetella bronchisepticaen_US
dc.typeArticleen_US
ecu.journal.issue4
ecu.journal.nameJournal of Bacteriology
ecu.journal.pages862-870
ecu.journal.volume180

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