Biology Reference
In-Depth Information
observed (
Kenny et al., 1996
;
Lai et al., 1997
), directly confirming that the
T3SS is functional. Additionally, deletion of individual LEE genes results in a
lack of A/E lesion formation and reduced virulence (
Rosenshine et al., 1992
;
Kenny and Finlay, 1995
;
Tacket et al., 2000
).
Evolutionary, the T3SS encoded in the EPEC LEE is most closely related to
the
Salmonella typhimurium
SPI-2 T3SS, as determined by sequence similarity
(
Hensel et al., 1998
), which is active only in the
Salmonella
-containing vacu-
ole. It remains to be seen if this phylogenetic proximity corresponds to similar
features between these two systems, or if it simply reflects a common origin.
The Mxi/Spa system of
Shigella
The main determinant of virulence in pathogenic
Shigella flexneri
is the pres-
ence of the large virulence plasmid pWR100 (
Sansonetti et al., 1982, 1983
),
a 200 kb plasmid encoding for approximately 100 genes (
Venkatesan et al.,
2001
). It is found in all pathogenic serotypes of
S. flexneri
,
S. dysenteriae
and
S. sonnei
(
Yang et al., 2005
), and is necessary for pathogenicity. Importantly,
this plasmid can confer invasive properties to non-pathogenic
E. coli
strains
(
Sansonetti et al., 1983
) and can be transmitted between bacteria (
Sansonetti
et al., 1982
).
Within this plasmid, a 31 kb pathogenicity island was identified (
Sasakawa
et al., 1988
), and sequence analysis showed that it contains 34 genes organized
in two clusters transcribed in opposite directions (
Figure 14.1
B). Subsequent
studies demonstrated that it forms a functional T3SS (
Menard et al., 1994
),
labeled the Mxi/Spa system. It is one of the best-conserved regions of the viru-
lence plasmid (
Yang et al., 2005
) and is necessary for epithelial cell invasion
and macrophage killing (
Sansonetti, 1991
;
Zychlinsky et al., 1992
).
The Mxi/Spa system is closely related to the well-studied
inv
system, the
Salmonella typhimurium
SPI-1 encoded T3SS (
Troisfontaines and Cornelis,
2005
), which is responsible for the invasion into epithelial cells, suggesting a
similar role for these two T3SSs.
The ETT2 system
More recently, sequence for a putative second T3SS was identified in the
genome of the EHEC strain O157:H7 Sakai (
Ohnishi et al., 2000
), the source
of a food-borne
E. coli
outbreak in Japan in 1999. This system, called ETT2
(
E
. coli
T
ype
T
Three secretion
2
), was subsequently found in many EPEC and
EHEC strains (
Hartleib et al., 2003
;
Makino et al., 2003
). Deletion of the ETT2
reduces pathogenicity (
Ideses et al., 2005
;
Yao et al., 2009
), but the molecu-
lar aspects of this effect remain unclear. In particular, secretion has not been
observed to date for this system.
The ETT2 is formed by two separate operons, located in distinct loci of the
genome (
Ren et al., 2004
): the
epr/epi/eiv
operon contains 19 genes, coding
Search WWH ::
Custom Search