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recent studies on the
Shigella
T3SS indicate that the translocon proteins IpaB
and IpaD are key to host cell sensing (
Veenendaal et al., 2007
). This impor-
tant observation indicates that at least in some systems, the injectisome is fully
assembled prior to contact with the infected cell. This suggests that cell contact-
dependent induction of secretion does not occur at the genetic level, but through
an unknown signaling pathway, similar to the various substrate switching events
observed during assembly.
Similarly, a number of environmental factors have been reported to influ-
ence the level of secretion, which varies in different systems. In EPEC, secre-
tion of the LEE T3SS is maximal at 37°C, pH 7, and in the presence of sodium
bicarbonate, calcium and Fe(NO
3
)
3
(
Kenny et al., 1997
); these conditions are
thought to correspond to the conditions in which T3S occurs
in vivo
. Similarly,
the T3SS of
Shigella
is induced under anaerobic conditions, similar to the envi-
ronment of cellular invasion during an infection (
Marteyn et al., 2010
). How-
ever, inducing conditions do not necessarily reflect the
in vivo
situation; for
instance, in
Shigella
T3S can be induced
in vitro
by the addition of Congo red
to the growth media (
Bahrani et al., 1997
).
Finally, quorum sensing has been shown to be an important factor in T3SS
regulation. Quorum sensing, a process used by bacteria to communicate with
one another (
Bassler and Losick, 2006
), is based on the secretion of partic-
ular small molecules (termed auto-inducers) into the media surrounding the
bacteria, a chemical cross-talk which can be detected by others, and lead to
appropriate changes in gene transcription. In EPEC and EHEC, it has been
shown that the
luxS
gene, responsible for the production of the auto-inducers
AI-2 and AI-3, controls the transcription of the LEE genes (
Sperandio et al.,
1999
) through a complex cascade involving the QseBC and QseDEFG path-
ways (
Antunes et al., 2010
).
Genetic regulation of the LEE
All T3SSs encode regulatory genes that allow the synchronized transcription
of the various genes in the system. However, these regulatory genes and their
regulated transcription differ significantly depending on the system.
The LEE-encoded
ler
gene is a critical regulator of LEE transcription
(
Mellies et al., 1999
), as it activates the transcription of the LEE2, LEE3,
LEE4, and LEE5 operons (
Figure 14.1
A). Ler is homologous to the transcrip-
tional repressor H-NS (a general housekeeping protein involved in many bac-
terial processes; see
Dorman, 2004
for review). Ler is suggested to function
by competing with and relieving the transcriptional repression of H-NS within
the LEE (
Bustamante et al., 2001
). Importantly,
ler
transcription is itself regu-
lated by a number of factors, including quorum sensing and the SOS response
triggered by DNA damage (
Sperandio et al., 2000
). In addition, the PerC pro-
tein, a member of the AraC transcription factor family encoded in the EAF
plasmid found in EPEC strains, has been shown to activate the transcription of
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