Abstract
Salmonella enterica
serovar Typhimurium initiates infection of a host by inducing its own uptake into specialized M cells which reside within the epithelium overlaying Peyer's patches. Entry of
Salmonella
into intestinal epithelial cells is dependent upon invasion genes that are clustered together in
Salmonella
pathogenicity island 1 (SPI-1). Upon contact between serovar Typhimurium and epithelial cells targeted for bacterial internalization, bacterial proteins are injected into the host cell through a type III secretion system that leads to internalization of the bacteria. Previous work has established that the
prgH
, -
I
, -
J
, and -
K
and
orgA
genes reside in SPI-1, and the products of these genes are predicted to be components of the invasion secretion apparatus. We report that an error in the published
orgA
DNA sequence has been identified so that this region encodes two small genes rather than a single large open reading frame. These genes have been designated
orgA
and
orgB
. Additionally, an opening reading frame downstream of
orgB
, which we have designated
orgC
, has been identified and partially characterized. Previously published work has indicated that the
prgH
, -
I
, -
J
, and -
K
genes are transcribed from a promoter distinct from that used by the gene immediately downstream,
orgA
. Here, we present experiments indicating that
orgA
expression is driven by the
prgH
promoter. In addition, using reverse transcriptase PCR analysis, we have found that this polycistronic message extends downstream of
prgH
to include a total of 10 genes. To more fully characterize this invasion operon, we demonstrate that the
prgH
,
prgI
,
prgJ
,
prgK
,
orgA
, and
orgB
genes are each required for invasion and secretion, while
orgC
is not essential for the invasive phenotype.