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Co‐ordination of pathogenicity island expression by the BipA GTPase in enteropathogenic Escherichia coli (EPEC)
Author(s) -
Grant Andrew J.,
Farris Michele,
Alefounder Peter,
Williams Peter H.,
Woodward Martin J.,
O'Connor C. David
Publication year - 2003
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.2003.t01-1-03447.x
Subject(s) - intimin , biology , pathogenicity island , enteropathogenic escherichia coli , bacterial adhesin , virulence , microbiology and biotechnology , flagellum , type three secretion system , gtpase , effector , pilus , escherichia coli , virulence factor , genetics , gene , enterobacteriaceae
Summary BipA is a novel member of the ribosome binding GTPase superfamily and is widely distributed in bacteria and plants. We report here that it regulates multiple cell surface‐ and virulence‐associated components in the enteropathogenic Escherichia coli (EPEC) strain E2348/69. The regulated components include bacterial flagella, the espC pathogenicity island and a type III secretion system specified by the locus of enterocyte effacement (LEE). BipA positively regulated the espC and LEE gene clusters through transcriptional control of the L EE‐ e ncoded r egulator, Ler. Additionally, it affected the pattern of proteolysis of intimin, a key LEE‐encoded adhesin specified by the LEE. BipA control of the LEE operated independently of the previously characterized regulators Per, integration host factor and H‐NS. In contrast, it negatively regulated the flagella‐mediated motility of EPEC and in a Ler‐independent manner. Our results indicate that the BipA GTPase functions high up in diverse regulatory cascades to co‐ordinate the expression of key pathogenicity islands and other virulence‐associated factors in E. coli .