The non-pathogenic Escherichia coli strain W secretes SslE via the virulence-associated type II secretion system beta

BMC Microbiology

Research Article

Rembrandt J F Haft¹  Mark S DeCanio²  Robert Landick³ 

[1] Great Lakes Bioenergy Research Center, University of Wisconsin-Madison, Madison, WI, USA;Great Lakes Bioenergy Research Center, University of Wisconsin-Madison, Madison, WI, USA;Department of Biochemistry, University of Wisconsin-Madison, Madison, WI, USA;Great Lakes Bioenergy Research Center, University of Wisconsin-Madison, Madison, WI, USA;Department of Biochemistry, University of Wisconsin-Madison, Madison, WI, USA;Department of Bacteriology, University of Wisconsin-Madison, Madison, WI, USA;

关键词: Type II secretion;    Surface display;    Escherichia coli;    Colonization factor;   

DOI  :  10.1186/1471-2180-13-130

 received in 2013-03-11, accepted in 2013-06-04,  发布年份 2013

来源: Springer

【 摘 要 】

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.

【 授权许可】

Unknown   
© DeCanio et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.