Enteropathogenic Escherichia coli (EPEC) is a diarrheagenic bacterium that predominantly infects infants in developing countries. EPEC forms attaching and effacing (A/E) lesions on the apical surface of the small intestine, leading to diarrhea. The locus of enterocyte effacement (LEE) is both necessary and sufficient for A/E lesion morphogenesis by EPEC. Gene expression from this virulence determinant is controlled by an elaborate regulatory web that extends beyond protein-based transcriptional regulators and includes small regulatory RNA (sRNA) that exert their effects posttranscriptionally. To date, only 4 Hfq-dependent sRNAs-MgrR, RyhB, McaS, and Spot42-have been identified that affect the LEE of EPEC by diverse mechanisms and elicit varying regulatory outcomes. In this study, we demonstrate that the paralogous Hfq-dependent sRNAs OmrA and OmrB globally silence the LEE to diminish the ability of EPEC to form A/E lesions. Interestingly, OmrA and OmrB do not appear to directly target a LEE-encoded gene; rather, they repress transcription from the LEE1 promoter indirectly, by means of an as-yet-unidentified transcriptional factor that binds within 200 base pairs upstream of the transcription start site to reduce the expression of the LEE master regulator Ler, which, in turn, leads to reduced morphogenesis of A/E lesions. Additionally, OmrA and OmrB also repress motility in EPEC by targeting the 5' UTR of the flagellar master regulator, flhD.

• MeSH
• Coloring Agents MeSH
• Enteropathogenic Escherichia coli * MeSH
• Infant MeSH
• Humans MeSH
• Promoter Regions, Genetic MeSH
• Diarrhea MeSH
• Transcription Factors MeSH
• Check Tag
• Infant MeSH
• Humans MeSH
• Publication type
• Journal Article MeSH