Abstract
BackgroundMany pathogenic E. coli strains secrete virulence factors using type II secretory systems, homologs of which are widespread in Gram-negative bacteria. Recently, the enteropathogenic Escherichia coli strain E2348/69 was shown to secrete and surface-anchor SslE, a biofilm-promoting virulence factor, via a type II secretion system. Genes encoding SslE and its associated secretion system are conserved in some non-pathogenic E. coli, including the commonly-used W (Waksman) strain.ResultsWe report here that E. coli W uses its type II secretion system to export a cognate SslE protein. SslE secretion is temperature- and nutrient-dependent, being robust at 37°C in rich medium but strongly repressed by lower temperatures or nutrient limitation. Fusing either of two glycosyl hydrolases to the C-terminus of SslE prevented it from being secreted or surface-exposed. We screened mutations that inactivated the type II secretion system for stress-related phenotypes and found that inactivation of the secretion system conferred a modest increase in tolerance to high concentrations of urea. Additionally, we note that the genes encoding this secretion system are present at a hypervariable locus and have been independently lost or gained in different lineages of E. coli.ConclusionsThe non-pathogenic E. coli W strain shares the extracellular virulence factor SslE, and its associated secretory system, with pathogenic E. coli strains. The pattern of regulation of SslE secretion we observed suggests that SslE plays a role in colonization of mammalian hosts by non-pathogenic as well as pathogenic E. coli. Our work provides a non-pathogenic model system for the study of SslE secretion, and informs future research into the function of SslE during host colonization.
Highlights
Many pathogenic E. coli strains secrete virulence factors using type II secretory systems, homologs of which are widespread in Gram-negative bacteria
Type II secretion has been extensively studied in pathogenic strains of Escherichia coli, which collectively are known to use two distinct disease-promoting Type II secretion systems (T2SS): the StcE secreting system encoded by the pO157 virulence plasmid [7], and the heat-labile enterotoxin (LT) secreting system common to many pathogenic strains [8]
We found a strong effect of growth conditions on SslE secretion, which is relatively robust in rich medium at 37°C and undetectable when cells are cultured at 30°C or in minimal medium
Summary
Many pathogenic E. coli strains secrete virulence factors using type II secretory systems, homologs of which are widespread in Gram-negative bacteria. Type II secretion has been extensively studied in pathogenic strains of Escherichia coli, which collectively are known to use two distinct disease-promoting T2SS: the StcE secreting system encoded by the pO157 virulence plasmid [7], and the heat-labile enterotoxin (LT) secreting system common to many pathogenic strains [8]. The latter T2SS was shown for the first time to secrete a non-LT protein, known as SslE, from the enteropathogenic strain E2348/69, thereby promoting biofilm maturation and rabbit colonization by E2348/69 [9,10]. Based on phylogenetic and structural analyses, Dunstan et al recently determined that the E. coli T2SSβ is part of a larger group of T2SS that contain “Vibrio-type secretins”, making it a model for numerous type II secretion systems used to deliver toxic substrates by Vibrio and Escherichia species [10]
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