Laboratory adapted Escherichia coli K‐12 becomes a pathogen of Caenorhabditis elegans upon restoration of O antigen biosynthesis. Issue 5 (28th January 2013)

• Record Type: Journal Article
• Authors: Browning, Douglas F.; Wells, Timothy J.; França, Fernanda L. S.; Morris, Faye C.; Sevastsyanovich, Yanina R.; Bryant, Jack A.; Johnson, Matthew D.; Lund, Peter A.; Cunningham, Adam F.; Hobman, Jon L.; May, Robin C.; Webber, Mark A.; Henderson, Ian R.
• Is Part Of: Molecular microbiology. Volume 87:Issue 5(2013)
• Page Start: 939
• Page End: 950
• Publication Date: 2013-01-28
• Subjects: Molecular microbiology -- Periodicals; 572.829
• DOI: 10.1111/mmi.12144
• Languages: English
• ISSNs: 0950-382X

Abstract

<abstract abstract-type="main"> <title>Summary</title> <p> <italic>Escherichia coli</italic> has been the leading model organism for many decades. It is a fundamental player in modern biology, facilitating the molecular biology revolution of the last century. The acceptance of <italic>E. coli</italic> as model organism is predicated primarily on the study of one <italic>E. coli</italic> lineage; <italic>E. coli</italic> K‐12. However, the antecedents of today's laboratory strains have undergone extensive mutagenesis to create genetically tractable offspring but which resulted in loss of several genetic traits such as O antigen expression. Here we have repaired the <italic>wbbL</italic> locus, restoring the ability of <italic>E. coli</italic> K‐12 strain MG1655 to express the O antigen. We demonstrate that O antigen production results in drastic alterations of many phenotypes and the density of the O antigen is critical for the observed phenotypes. Importantly, O antigen production enables laboratory strains of <italic>E. coli</italic> to enter the gut of the <italic>Caenorhabditis elegans</italic> worm and to kill <italic>C. elegans</italic> at rates similar to pathogenic bacterial species. We demonstrate <italic>C. elegans</italic> killing is a feature of other commensal <italic>E. coli</italic>. We show killing is associated with bacterial resistance to mechanical shear and persistence in the <italic>C. elegans</italic> gut. These results suggest <italic>C. elegans</italic> is not an effective model of human‐pathogenic <italic>E. coli</italic> infectious disease.</p> </abstract>