Affiliation:
1. Department of Bacteriology
2. Infectious Diseases Surveillance Center, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, Tokyo 162-8640, Japan
Abstract
ABSTRACT
The gene function of the locus of enterocyte effacement (LEE) is essential for full virulence of enterohemorrhagic
Escherichia coli
(EHEC). Strict control of LEE gene expression is mediated by the coordinated activities of several regulatory elements. We previously reported that the ClpX/ClpP protease positively controls LEE expression by down-regulating intracellular levels of GrlR, a negative regulator of LEE gene expression. We further revealed that the negative effect of GrlR on LEE expression was mediated through GrlA, a positive regulator of LEE expression. In this study, we found that the FliC protein, a major component of flagellar filament, was overproduced in
clpXP
mutant EHEC, as previously reported for
Salmonella
. We further found that FliC expression was reduced in a
clpXP grlR
double mutant. To determine the mediators of this phenotype, FliC protein levels in wild-type,
grlR
,
grlA
, and
grlR grlA
strains were compared. Steady-state levels of FliC protein were reduced only in the
grlR
mutant, suggesting that positive regulation of FliC expression by GrlR is mediated by GrlA. Correspondingly, cell motility was also reduced in the
grlR
mutant, but not in the
grlA
or
grlR grlA
mutant. Because overexpression of
grlA
from a multicopy plasmid strongly represses the FliC level, as well as cell motility, we conclude that GrlA acts as a negative regulator of flagellar-gene expression. The fact that an EHEC strain constitutively expressing FlhD/FlhC cannot adhere to HeLa cells leads us to hypothesize that GrlA-dependent repression of the flagellar regulon is important for efficient cell adhesion of EHEC to host cells.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
83 articles.
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