Novel Repressor of Escherichia coli O157:H7 Motility Encoded in the Putative Fimbrial Cluster OI-1
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ABSTRACTEscherichia coli
O157:H7 is a gastrointestinal pathogen that has become a serious public health concern, as it is associated with outbreaks and severe diseases such as hemolytic-uremic syndrome. The molecular basis of its greater virulence than that of other serotypes is not completely known. OI-1 is a putative fimbria-encoding genomic island that is found almost exclusively in O157:H7 Shiga toxin-producing
E. coli
strains and may be associated with the enhanced pathogenesis of these strains. In this study, we identified and characterized a novel repressor of flagellar synthesis encoded by OI-1. We showed that deletion of
Z0021
increased the motility of
E. coli
O157:H7, which correlated with an increase in flagellin production and enhanced assembly of flagella on the cell surface. In contrast, overexpression of
Z0021
inhibited motility. We demonstrated that Z0021 exerted its regulatory effects downstream of the transcription and translation of
flhDC
but prior to the activation of class II/III promoters. Furthermore, the master regulator of flagellar synthesis, FlhD
4
C
2
, was shown to be a high-copy suppressor of the nonmotile phenotype associated with elevated levels of Z0021—a finding consistent with Z0021-FlhD
4
C
2
being a potential regulatory complex. This work provides insight into the mechanism by which Z0021, which we have named
fmrA
, represses flagellar synthesis and is the first report of a fimbrial-operon-encoded inhibitor of motility in
E. coli
O157:H7.
