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J Bacteriol, April 1998, p. 1682-1690, Vol. 180, No. 7
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Characterization of the bvgR Locus of
Bordetella pertussis
Tod J.
Merkel,1,*
Cassia
Barros,1 and
Scott
Stibitz2
National Institute of Dental Research,
National Institutes of Health,1 and
Center for Biologics Evaluation and Research, U.S. Food and
Drug Administration,2 Bethesda, Maryland 20892
Received 17 October 1997/Accepted 24 January 1998
Bordetella pertussis, the causative agent of whooping
cough, produces a wide array of factors that are associated with its ability to cause disease. The expression and regulation of these virulence factors is dependent upon the bvg locus
(originally designated the vir locus), which encodes two
proteins: BvgA, a 23-kDa cytoplasmic protein, and BvgS, a 135-kDa
transmembrane protein. It is proposed that BvgS responds to
environmental signals and interacts with BvgA, a transcriptional
regulator which upon modification by BvgS binds to specific promoters
and activates transcription. An additional class of genes is repressed
by the bvg locus. Expression of this class, the
bvg-repressed genes (vrgs [for vir-repressed
genes]), is reduced under conditions in which expression of the
aforementioned bvg-activated virulence factors is maximal;
this repression is dependent upon the presence of an intact
bvgAS locus. We have previously identified a locus required for regulation of all of the known bvg-repressed genes in
B. pertussis. This locus, designated bvgR, maps
to a location immediately downstream of bvgAS. We have
undertaken deletion and complementation studies, as well as sequence
analysis, in order to identify the bvgR open reading frame
and identify the cis-acting sequences required for regulated expression of bvgR. Studies utilizing
transcriptional fusions of bvgR to the gene encoding
alkaline phosphatase have demonstrated that bvgR is
activated at the level of transcription and that this activation is
dependent upon an intact bvgAS locus.
*
Corresponding author. Mailing address: OIIB/NIDR/NIH,
Building 30, Rm. 303, 30 Convent Dr. MSC 4350, Bethesda, MD 20892-4350. Phone: (301) 496-6060. Fax: (301) 402-0396. E-mail:
merkel{at}yoda.nidr.nih.gov.
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