Affiliation:
1. Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305
Abstract
ABSTRACT
Salmonella
pathogenicity island 2 (SPI-2) encodes a putative, two-component regulatory system, SsrA-SsrB, which regulates a type III secretion system needed for replication inside macrophages and systemic infection in mice. The sensor and regulator homologs,
ssrAB
(
spiR
), and genes within the secretion system, including the structural gene
ssaH
, are transcribed after
Salmonella
enters host cells. We have studied the transcriptional regulation of
ssrAB
and the secretion system by using
gfp
fusions to the
ssrA
and
ssaH
promoters. We found that early transcription of
ssrA
, after entry into macrophages, is most efficient in the presence of OmpR. An
ompR
mutant strain does not exhibit replication within cultured macrophages. Furthermore, footprint analysis shows that purified OmpR protein binds directly to the
ssrA
promoter region. We also show that minimal medium, pH 4.5, induces SPI-2 gene expression in wild-type but not
ompR
mutant strains. We conclude that the type III secretion system of SPI-2 is regulated by OmpR, which activates expression of
ssrA
soon after
Salmonella
enters the macrophage.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
277 articles.
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