Article abstract
Nature Methods 5, 789 - 795 (2008)
Published online: 1 August 2008 | Corrected online: 17 August 2008 | doi:10.1038/nmeth.1239
eSGA: E. coli synthetic genetic array analysis
Gareth Butland1,2,7,8, Mohan Babu1,8, J Javier Díaz-Mejía1,3, Fedyshyn Bohdana1, Sadhna Phanse1, Barbara Gold2, Wenhong Yang2, Joyce Li1, Alla G Gagarinova4, Oxana Pogoutse1, Hirotada Mori5, Barry L Wanner5, Henry Lo1, Jas Wasniewski1, Constantine Christopoulos1, Mehrab Ali4, Pascal Venn1, Anahita Safavi-Naini1, Natalie Sourour1, Simone Caron1, Ja-Yeon Choi1, Ludovic Laigle1, Anaies Nazarians-Armavil1, Avnish Deshpande1, Sarah Joe1, Kirill A Datsenko6, Natsuko Yamamoto5, Brenda J Andrews1,4, Charles Boone1,5, Huiming Ding1, Bilal Sheikh1, Gabriel Moreno-Hagelsieb3, Jack F Greenblatt1,4 & Andrew Emili1,4
Abstract
Physical and functional interactions define the molecular organization of the cell. Genetic interactions, or epistasis, tend to occur between gene products involved in parallel pathways or interlinked biological processes. High-throughput experimental systems to examine genetic interactions on a genome-wide scale have been devised for Saccharomyces cerevisiae, Schizosaccharomyces pombe, Caenorhabditis elegans and Drosophila melanogaster, but have not been reported previously for prokaryotes. Here we describe the development of a quantitative screening procedure for monitoring bacterial genetic interactions based on conjugation of Escherichia coli deletion or hypomorphic strains to create double mutants on a genome-wide scale. The patterns of synthetic sickness and synthetic lethality (aggravating genetic interactions) we observed for certain double mutant combinations provided information about functional relationships and redundancy between pathways and enabled us to group bacterial gene products into functional modules.
NOTE: In the version of this article initially published online two author names (Gabriel Moreno-Hagelseib and Constantine Christopolous) were spelled incorrectly. The correct author names are Gabriel Moreno-Hagelsieb and Constantine Christopoulos. The error has been corrected for the print, PDF and HTML versions of this article.
- Banting and Best Department of Medical Research, Terrence Donnelly Centre for Cellular and Biomolecular Research, University of Toronto, 160 College Street, Toronto M5S 3E1, Canada.
- Life Sciences Division, Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, California 94720, USA.
- Department of Biology, Wilfrid Laurier University, 75 University Avenue West, Waterloo N2L 3C5, Canada.
- Department of Molecular Genetics, University of Toronto, 1 King's College Circle, Toronto M5S 1A8, Canada.
- Graduate School of Biological Sciences, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma, Nara 630-0101, Japan.
- Department of Biological Sciences, Purdue University, 915 W. State Street, West Lafayette, Indiana 47907, USA.
- Present address: Life Sciences Division, Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, California 94720, USA.
- These authors contributed equally to this work.
Correspondence to: Jack F Greenblatt1,4 e-mail: jack.greenblatt@utoronto.ca
Correspondence to: Andrew Emili1,4 e-mail: andrew.emili@utoronto.ca
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