OmpR coordinates the expression of virulence factors of Enterohemorrhagic Escherichia coli in the alimentary tract of Caenorhabditis elegans
Enterohemorrhagic Escherichia coli (EHEC), an enteropathogen that colonizes in the intestine, causes severe diarrhea and hemorrhagic colitis in humans by the expression of the type III secretion system (T3SS) and Shiga‐like toxins (Stxs). However, how EHEC can sense and respond to the changes in the...
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Veröffentlicht in: | Molecular microbiology 2021-07, Vol.116 (1), p.168-183 |
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Zusammenfassung: | Enterohemorrhagic Escherichia coli (EHEC), an enteropathogen that colonizes in the intestine, causes severe diarrhea and hemorrhagic colitis in humans by the expression of the type III secretion system (T3SS) and Shiga‐like toxins (Stxs). However, how EHEC can sense and respond to the changes in the alimentary tract and coordinate the expression of these virulence genes remains elusive. The T3SS‐related genes are known to be regulated by the locus of enterocyte effacement (LEE)‐encoded regulators, such as Ler, as well as non‐LEE‐encoded regulators in response to different environmental cues. Herein, we report that OmpR, which participates in the adaptation of E. coli to osmolarity and pH alterations, is required for EHEC infection in Caenorhabditis elegans. OmpR protein was able to directly bind to the promoters of ler and stx1 (Shiga‐like toxin 1) and regulate the expression of T3SS and Stx1, respectively, at the transcriptional level. Moreover, we demonstrated that the expression of ler in EHEC is in response to the intestinal environment and is regulated by OmpR in C. elegans. Taken together, we reveal that OmpR is an important regulator of EHEC which coordinates the expression of virulence factors during gastrointestinal infection in vivo.
Enterohemorrhagic Escherichia coli (EHEC) causes human diseases by the type III secretion system (T3SS) and Shiga‐like toxins (Stxs). Herein, we report that OmpR, which participates in the adaptation of E. coli to osmolarity and pH alterations, is also required for EHEC infection. We demonstrated that OmpR binds directly to the promoters of ler and stx1 in vitro and regulates the expression of T3SS and Stx1 in response to the intestinal environment in vivo. |
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ISSN: | 0950-382X 1365-2958 |
DOI: | 10.1111/mmi.14698 |