Involvement of PatE, a prophage-encoded AraC-like regulator, in the transcriptional activation of acid resistance pathways of enterohemorrhagic Escherichia coli strain EDL933

Enterohemorrhagic E. coli (EHEC) O157:H7 is a lethal human intestinal pathogen which causes hemorrhagic colitis and the hemolytic uremic syndrome. EHEC is transmitted by the fecal-oral route and has a lower infectious dose than most other enteric bacterial pathogens in that fewer than 100 cfu are able to cause disease. This low infectious dose has been attributed to the ability of EHEC to survive in the acidic environment of the human stomach. In-silico analysis of the genome of EHEC O157:H7 strain EDL933 revealed a gene, patE, for a putative AraC-like regulatory protein within the prophage island, CP-933H. Transcriptional analysis in E. coli showed that the expression of patE is induced during stationary phase. Data from microarray assays demonstrated that PatE activates the transcription of genes encoding proteins of acid resistance pathways. In addition, PatE down regulated the expression of a number of genes encoding heat-shock proteins and the type III secretion pathway of EDL933. Transcriptional analysis and electrophoretic mobility shift assays suggested that PatE also activates the transcription of the gene for the acid-stress chaperone, hdeA, by binding to its promoter region. Finally, assays of acid tolerance showed that increasing the expression of PatE in EHEC greatly enhanced the ability of the bacteria to survive in different acidic environments. Together these findings indicate that EHEC strain EDL933 carries a prophage-encoded regulatory system which contributes to acid resistance.