Lethal paralysis of Caenorhabditis elegans by Pseudomonasaeruginosa
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Communicated by A. Dale Kaiser, Stanford University School of Medicine, Stanford, CA (received for review August 23, 1999)
Abstract
Identification of host factors that interact with pathogens is crucial to an understanding of infectious disease, but direct screening for host mutations to aid in this task is not feasible in mammals. The nematode Caenorhabditis elegans is a genetically tractable alternative for investigating the pathogenic bacterium Pseudomonas aeruginosa. A P. aeruginosa toxin, produced at high cell density under control of the quorum-sensing regulators LasR and RhlR, rapidly and lethally paralyzes C. elegans. Loss-of-function mutations in C. elegans egl-9, a gene required for normal egg laying, confer strong resistance to the paralysis. Thus, activation of EGL-9 or of a pathway that includes it may lead to the paralysis. The molecular identity of egl-9 was determined by transformation rescue and DNA sequencing. A mammalian homologue of EGL-9 is expressed in tissues in which exposure to P. aeruginosa could have clinical effects.
Footnotes
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↵ * Present address: Department of Microbiology and Immunology, Stanford University Medical School, Stanford, CA 94305.
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↵ † To whom reprint requests should be addressed. E-mail: manoil{at}u.washington.edu.
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Data deposition: The sequence reported in this paper has been deposited in the GenBank database (accession no. AF178536).
- Abbreviations:
- YAC,
- yeast artificial chromosome;
- kb,
- kilobase;
- GFP,
- green fluorescent protein
- Copyright © 1999, The National Academy of Sciences
