Detection and avoidance of a natural product from the pathogenic bacterium Serratia marcescens by Caenorhabditis elegans
- Elizabeth Pradel*,†,‡,§,
- Yun Zhang¶,‖,
- Nathalie Pujol*,†,‡,
- Tohey Matsuyama**,
- Cornelia I. Bargmann¶,††, and
- Jonathan J. Ewbank*,†,‡,††
- *Centre d'Immunologie de Marseille-Luminy, Université de la Méditerranée, Case 906, 13288 Marseille Cedex 9, France;
- †Institut National de la Santé et de la Recherche Médicale, U631, 13288 Marseille, France;
- ‡Centre National de la Recherche Scientifique, Unité Mixte de Recherche 6102, 13288 Marseille, France;
- ¶Howard Hughes Medical Institute, The Rockefeller University, 1230 York Avenue, New York, NY 10021; and
- **Department of Infectious Disease Control and International Medicine, Niigata University Graduate School of Medical and Dental Sciences, Niigata 951-8510, Japan
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Contributed by Cornelia I. Bargmann, November 22, 2006 (received for review November 13, 2006)
Abstract
The nematode Caenorhabditis elegans is present in soils and composts, where it can encounter a variety of microorganisms. Some bacteria in these rich environments are innocuous food sources for C. elegans, whereas others are pathogens. Under laboratory conditions, C. elegans will avoid certain pathogens, such as Serratia marcescens, by exiting a bacterial lawn a few hours after entering it. By combining bacterial genetics and nematode genetics, we show that C. elegans specifically avoids certain strains of Serratia based on their production of the cyclic lipodepsipentapeptide serrawettin W2. Lawn-avoidance behavior is chiefly mediated by the two AWB chemosensory neurons, probably through G protein-coupled chemoreceptors, and also involves the nematode Toll-like receptor gene tol-1. Purified serrawettin W2, added to an Escherichia coli lawn, can directly elicit lawn avoidance in an AWB-dependent fashion, as can another chemical detected by AWB. These findings represent an insight into chemical recognition between these two soil organisms and reveal sensory mechanisms for pathogen recognition in C. elegans.
Footnotes
- ††To whom correspondence may be addressed. E-mail: cori{at}rockefeller.edu or ewbank{at}ciml.univ-mrs.fr
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↵ §Present address: Institut National de la Santé et de la Recherche Médicale, U801, Institut Pasteur de Lille, IBL BP447, 59021 Lille Cedex, France.
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↵ ‖Present address: Department of Organismic and Evolutionary Biology, Center for Brain Science, Harvard University, 26 Oxford Street, Cambridge, MA 02138.
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Author contributions: E.P. and Y.Z. contributed equally; E.P., Y.Z., C.I.B., and J.J.E. designed research; E.P., Y.Z., N.P., T.M., and J.J.E. performed research; T.M. contributed new reagents/analytic tools; E.P., Y.Z., C.I.B., and J.J.E. analyzed data; and C.I.B. and J.J.E. wrote the paper.
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The authors declare no conflict of interest.
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Freely available online through the PNAS open access option.
- © 2007 by The National Academy of Sciences of the USA





