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Characterization of a novel microcin that kills enterohemorrhagic Escherichia coli O157:H7 and O26.

Authors
  • Eberhart, Lauren J1
  • Deringer, James R
  • Brayton, Kelly A
  • Sawant, Ashish A
  • Besser, Thomas E
  • Call, Douglas R
  • 1 Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, Washington, USA.
Type
Published Article
Journal
Applied and Environmental Microbiology
Publisher
American Society for Microbiology
Publication Date
Sep 01, 2012
Volume
78
Issue
18
Pages
6592–6599
Identifiers
DOI: 10.1128/AEM.01067-12
PMID: 22773653
Source
Medline
License
Unknown

Abstract

A novel phenotype was recently identified in which specific strains of Escherichia coli inhibit competing E. coli strains via a mechanism that was designated "proximity-dependent inhibition" (PDI). PDI-expressing (PDI(+)) E. coli is known to inhibit susceptible (PDI(-)) E. coli strains, including several enterohemorrhagic (EHEC) and enterotoxigenic (ETEC) E. coli strains. In this study, every strain from a genetically diverse panel of E. coli O157:H7 (n = 25) and additional strains of E. coli serovar O26 were susceptible to the PDI phenotype. LIVE/DEAD staining was consistent with inhibition by killing of susceptible cells. Comparative genome analysis identified the genetic component of PDI, which is composed of a plasmid-borne (Incl1) operon encoding a putative microcin and associated genes for transport, immunity, and microcin activation. Transfer of the plasmid to a PDI(-) strain resulted in transfer of the phenotype, and deletion of the genes within the operon resulted in loss of the inhibition phenotype. Deletion of chromosomally encoded tolC also resulted in loss of the inhibitory phenotype, and this confirmed that the putative microcin is most likely secreted via a type I secretion pathway. Deletion of an unrelated plasmid gene did not affect the PDI phenotype. Quantitative reverse transcription (RT)-PCR demonstrated that microcin expression is correlated with logarithmic-phase growth. The ability to inhibit a diversity of E. coli strains indicates that this microcin may influence gut community composition and could be useful for control of important enteric pathogens.

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