1887

Abstract

Enterohaemorrhagic (EHEC) is a life-threatening human pathogen worldwide. The locus of enterocyte effacement (LEE) in EHEC encodes a type three secretion system and effector proteins, all of which are essential for bacterial adherence to host cells. When LEE expression is activated, flagellar gene expression is down-regulated because bacterial flagella induce the immune responses of host cells at the infection stage. Therefore, this inverse regulation is also important for EHEC infection. We report here that a small regulatory RNA (sRNA), Esr41, mediates LEE repression and flagellar gene activation. Multiple copies of abolished LEE expression by down-regulating the expression of and , which encode positive regulators of LEE. This regulation led to reduced EHEC adhesion to host cells. Translational gene-reporter fusion experiments revealed that Esr41 regulates expression at a post-transcriptional level, and transcription, probably via an unknown target of Esr41. Esr41-mediated and repression was not observed in cells lacking , which encodes an RNA-binding protein essential for most sRNA functions, indicating that Esr41 acts in an Hfq-dependent manner. We previously reported an increase in cell motility induced by Esr41. This motility enhancement was also observed in EHEC lacking , showing that Esr41-mediated enhancement of cell motility is in a independent manner. In addition, Esr41 activated the expression of flagellar Class 3 genes by indirectly inducing the transcription of , which encodes the sigma factor for flagellar synthesis. These results suggest that Esr41 plays important roles in the inverse regulation of LEE and flagellar gene expression.

Keyword(s): EHEC , flagellar , LEE and small RNA
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2018-05-01
2024-04-23
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