Affiliation:
1. Department of Microbiology and Immunology, East Carolina University School of Medicine, Greenville, North Carolina 27858-4354
Abstract
ABSTRACT
A
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
Kpn
I-
Pst
I
Bordetella pertussis
DNA fragment mapping downstream of the alcaligin biosynthesis genes
alcABC
restored both siderophore biosynthesis and expression of the iron-regulated 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.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
42 articles.
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