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.
