ID31336143
Published Date2019-10-01
JournalMicrobial pathogenesis, 2019-10-01, Volume 135 Find other publications in this journal
Author Info
  • Department of Biology, Saint Joseph's University, 5600 City Avenue, Philadelphia, 19131, PA, USA; Department of Microbiology, University of Pennsylvania, 3610 Hamilton Walk, Philadelphia, 19104, PA, USA.
  • Department of Biology, Saint Joseph's University, 5600 City Avenue, Philadelphia, 19131, PA, USA.
  • Department of Neuroscience, New York State Psychiatric Institute, Columbia University Medical Center, New York, 10032, USA.
  • Department of Pathology and Laboratory Medicine, Emory University, Atlanta, 30341, GA, USA.
  • Department of Biology, Saint Joseph's University, 5600 City Avenue, Philadelphia, 19131, PA, USA. Electronic address: sbhatt@sju.edu.

Abstract

The diarrheic bacterium Escherichia albertii is a recent addition to the attaching and effacing (A/E) morphotype of pathogens. A/E pathogens cause disease by tightly attaching to intestinal cells, destroying their actin-rich microvilli, and triggering re-localization and repolymerization of actin at the bacterial-host interface to form actin-filled membranous protrusions, termed A/E lesions, beneath the adherent bacterium. The locus of enterocyte effacement (LEE) is required for the biogenesis of these lesions. Whereas regulation of the LEE has been intensively investigated in EPEC and EHEC, it remains cryptic in E. albertii. In this study we characterized the very first transcriptional and posttranscriptional regulators of the LEE in this emerging pathogen. Our results suggest that Ler and GrlA globally activate transcription from the LEE, whereas GrlR negatively regulates the LEE. Additionally, we demonstrate that the RNA chaperone Hfq posttranscriptionally represses the LEE by specifically targeting the 5' UTR of grlR. In summary, our findings provide the very first glimpse of the regulatory landscape of the LEE in E. albertii - a bacterium that has been implicated in multiple diarrheal outbreaks worldwide.