These authors contributed equally to this work. The authors declare no conflict of interest.
Laboratory adapted Escherichia coli K-12 becomes a pathogen of Caenorhabditis elegans upon restoration of O antigen biosynthesis
Article first published online: 28 JAN 2013
© 2013 Blackwell Publishing Ltd
Volume 87, Issue 5, pages 939–950, March 2013
How to Cite
Browning, D. F., Wells, T. J., França, F. L. S., Morris, F. C., Sevastsyanovich, Y. R., Bryant, J. A., Johnson, M. D., Lund, P. A., Cunningham, A. F., Hobman, J. L., May, R. C., Webber, M. A. and Henderson, I. R. (2013), Laboratory adapted Escherichia coli K-12 becomes a pathogen of Caenorhabditis elegans upon restoration of O antigen biosynthesis. Molecular Microbiology, 87: 939–950. doi: 10.1111/mmi.12144
- Issue published online: 24 FEB 2013
- Article first published online: 28 JAN 2013
- Manuscript Accepted: 20 DEC 2012
- from the Medical Research Council
Escherichia coli 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 E. coli as model organism is predicated primarily on the study of one E. coli lineage; E. coli 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 wbbL locus, restoring the ability of E. coli 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 E. coli to enter the gut of the Caenorhabditis elegans worm and to kill C. elegans at rates similar to pathogenic bacterial species. We demonstrate C. elegans killing is a feature of other commensal E. coli. We show killing is associated with bacterial resistance to mechanical shear and persistence in the C. elegans gut. These results suggest C. elegans is not an effective model of human-pathogenic E. coli infectious disease.