Laboratory adapted Escherichia coli K-12 becomes a pathogen of Caenorhabditis elegans upon restoration of O antigen biosynthesis

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@article{9ce5a716ef9b46a4a0578584bbacf1be,
title = "Laboratory adapted Escherichia coli K-12 becomes a pathogen of Caenorhabditis elegans upon restoration of O antigen biosynthesis",
abstract = "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.",
author = "Browning, {Douglas F} and Wells, {Timothy J} and Fran{\c c}a, {Fernanda L S} and Morris, {Faye C} and Sevastsyanovich, {Yanina R} and Bryant, {Jack A} and Johnson, {Matthew D} and Lund, {Peter A} and Cunningham, {Adam F} and Hobman, {Jon L} and May, {Robin C} and Webber, {Mark A} and Henderson, {Ian R}",
note = "{\textcopyright} 2013 Blackwell Publishing Ltd.",
year = "2013",
month = mar,
doi = "10.1111/mmi.12144",
language = "English",
volume = "87",
pages = "939--50",
journal = "Molecular Microbiology",
issn = "0950-382X",
publisher = "Wiley",
number = "5",

}

RIS

TY - JOUR

T1 - Laboratory adapted Escherichia coli K-12 becomes a pathogen of Caenorhabditis elegans upon restoration of O antigen biosynthesis

AU - Browning, Douglas F

AU - Wells, Timothy J

AU - França, Fernanda L S

AU - Morris, Faye C

AU - Sevastsyanovich, Yanina R

AU - Bryant, Jack A

AU - Johnson, Matthew D

AU - Lund, Peter A

AU - Cunningham, Adam F

AU - Hobman, Jon L

AU - May, Robin C

AU - Webber, Mark A

AU - Henderson, Ian R

N1 - © 2013 Blackwell Publishing Ltd.

PY - 2013/3

Y1 - 2013/3

N2 - 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.

AB - 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.

U2 - 10.1111/mmi.12144

DO - 10.1111/mmi.12144

M3 - Article

C2 - 23350972

VL - 87

SP - 939

EP - 950

JO - Molecular Microbiology

JF - Molecular Microbiology

SN - 0950-382X

IS - 5

ER -