The small regulatory RNA DsrA silences the locus of enterocyte effacement of enteropathogenic Escherichia coli in an RpoS-dependent manner

TL;DR

The sRNA DsrA silences the LEE in EPEC by repressing Ler through RpoS, showing a different regulatory role compared to EHEC.

Contribution

DsrA is identified as a novel riboregulator of the LEE in EPEC, acting in an RpoS-dependent manner.

Findings

DsrA globally silences the LEE by repressing the master regulator Ler in EPEC.

The repression of LEE1 is mediated through the sigma factor RpoS.

DsrA's regulatory role in EPEC contrasts with its activating role in EHEC.

Abstract

Attaching and effacing (A/E) pathogens adhere to intestinal cells (attachment) and destroy their microvilli (effacement). The A/E pathophenotype is encoded by a cluster of genes that are organized into the pathogenicity island called locus of enterocyte effacement (LEE). While transcriptional regulation of the LEE has been extensively interrogated in A/E pathogens, posttranscriptional regulation remains poorly understood. The RNA-binding protein Hfq and Hfq-dependent regulatory RNAs (sRNAs) play important roles in regulating the LEE posttranscriptionally. In a recent screen, we identified the Hfq-dependent sRNA DsrA as a novel riboregulator of the LEE in the A/E pathogen enteropathogenic
Escherichia coli
. Our findings suggest that DsrA globally silences the LEE by negatively regulating transcription of the
LEE1
-encoded master regulator Ler. The repression of
LEE1
is mediated through the stationary phase sigma factor, RpoS. Interestingly, our results contrast with what has been previously reported on the role of DsrA in EHEC, where the sRNA activates transcription from the
LEE1
promoter in an RpoS-dependent manner. The contrasting regulatory role of DsrA in EPEC and EHEC underscores the need for experimental validation of sRNA networks within each lineage, rather than inferring their function based on their roles in related bacteria.

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