Abstract
Enterohemorrhagic Escherichia coli O157:H7 is a major human enteric pathogen capable of causing large outbreaks of severe infections that induce bloody diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome. Its genome contains 177 unique O islands (OIs) including those carrying the main virulence elements, Shiga toxin-converting phages (OI-45 and OI-93) and locus for enterocyte effacement (OI-148). However, many of these islands harbor only genes of unknown function. Here, we demonstrate that OI-29 encodes a newly discovered transcriptional activator, Z0639 (named GmrA), that is required for motility and flagellar synthesis in O157:H7. GmrA directly binds to the promoter of fliA, an RNA polymerase sigma factor, and thereby regulates flagellar genes controlled by FliA. Expression of gmrA is maximal under host conditions (37°C, neutral pH, and physiological osmolarity), and in the presence of host epithelial cells, indicative of a role of this gene in infection by promoting motility. Finally, GmrA was found to be a widespread regulator of bacterial motility and flagellar synthesis in different pathotypes of E. coli. Our work largely enriches our understanding of bacterial motility control, and provides another example of regulators acquired laterally that mediate flagellar synthesis.
Highlights
Enterohemorrhagic Escherichia coli (EHEC) is a principally foodborne pathogen linked to serious diseases, including hemorrhagic colitis and hemolytic uremic syndrome (Monteiro et al, 2016)
We demonstrate that Z0639, renamed as GmrA (Genomic island-encoded Motility Regulator A), encoded in O islands (OIs)-29 is a newly discovered transcriptional activator that regulates flagellar synthesis and motility in E. coli O157:H7
OI-29 Is Not Required for O157:H7 Adherence and LEE Gene Expression
Summary
Enterohemorrhagic Escherichia coli (EHEC) is a principally foodborne pathogen linked to serious diseases, including hemorrhagic colitis and hemolytic uremic syndrome (Monteiro et al, 2016). The induction of such lesions is most critical for the establishment of successful colonization to cause infection, and this ability is conferred by locus of OI-29 Controls E. coli Motility enterocyte effacement (LEE), which consists of five polycistronic operons (LEE1 to LEE5) encoding a type III secretion system and associated effectors (Wong et al, 2011; Monteiro et al, 2016) Gene expression from this locus is regulated via a complex mechanism to ensure the expression occurs only under host conditions (Mellies et al, 2007; Connolly et al, 2015). While LEE1-encoded ler is the master activator of all LEE operons, a range of global and specific regulators are involved, such as H-NS, IHF, QseA, GrvA, GadE, Pch, EivF, EtrA, and Hha (Connolly et al, 2015)
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