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(a)
CRP
glucose
cAMP
RNA pol
-35
-10
eltA
eltB
(b)
CRP-cAMP
4
-35
-10
eltA
eltB
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-3
5
FIGURE 6.1
Modulation of LT gene transcription by CRP provides an example of catabolite
activation in ETEC. (a) At high glucose concentrations, cAMP levels in the cell are low and the
homodimeric CRP molecule (shown with four potential cAMP binding sites) is inactive allowing
RNA polymerase to interact with the promoter region and initiate transcription of
eltA
. (b) At low
glucose concentrations, cAMP levels in the bacteria increase, activating CRP and permitting the
CRP-cAMP complex to bind to a CRP binding site (operator centered at -31.5 upstream from
eltA
)
within the
eltA
promoter region. This prevents transcription by preventing the RNA polymerase
from forming an open complex at the promoter.
(Adapted from
Bodero and Munson (2009)
.)
Interestingly, intestinal epithelial cells possess high-affinity cAMP
transporters that efflux cAMP into the surrounding milieu (
Li et al., 2007
) as
cAMP levels in the host cell increase. Therefore it is intriguing to hypothesize
that ETEC actually sense cAMP generated by target epithelial cells in response
to successful delivery of LT, ultimately governing the interaction of ETEC and
target epithelium.
Rns and CfaD
Two other transcriptional regulators, Rns (
Caron et al., 1989
) and CfaD, have
been shown to modulate expression of virulence genes in ETEC. Both belong
to the AraC/XylS family of transcriptional regulators and their amino acid
sequences are 95% identical (
Pilonieta et al., 2007
). CfaD, located on the large
vate production of CFA/I (
Jordi et al., 1992
), while Rns is known to activate
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