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EMBO reports 6, 10, 992–997 (2005)
doi:10.1038/sj.embor.7400516
Published online: 9 September 2005
Yersinia pestis kills Caenorhabditis elegans by a biofilm-independent process that involves novel virulence factors
Katie L Styer1, Gregory W Hopkins2, Sara Schesser Bartra3, Gregory V Plano3, Richard Frothingham2 & Alejandro Aballay1
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1 Department of Molecular Genetics & Microbiology, 268 Jones Building, Box 3054 DUMC, Duke University Medical Center, Durham, North Carolina 27710, USA
2 Department of Medicine, Box 3230 DUMC, Duke University Medical Center, Durham, North Carolina 27710, USA
3 Department of Microbiology & Immunology, Room 3045A, Rosenstiel Medical Sciences Building, University of Miami School of Medicine, 1600 NW Tenth Avenue, Miami, Florida 33136, USA
To whom correspondence should be addressed
Alejandro Aballay Tel: +1 919 681 6765; Fax: +1 919 684 2790; E-mail: a.aballay@duke.edu
Received 28 February 2005; Accepted 2 August 2005; Published online 9 September 2005.
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Abstract
It is known that Yersinia pestis kills Caenorhabditis elegans by a biofilm-dependent mechanism that is similar to the mechanism used by the pathogen to block food intake in the flea vector. Using Y. pestis KIM5, which lacks the genes that are required for biofilm formation, we show that Y. pestis can kill C. elegans by a biofilm-independent mechanism that correlates with the accumulation of the pathogen in the intestine. We used this novel Y. pestis–C. elegans pathogenesis system to show that previously known and unknown virulence-related genes are required for full virulence in C. elegans. Six Y. pestis mutants with insertions in genes that are not related to virulence before were isolated using C. elegans. One of the six mutants carried an insertion in a novel virulence gene and showed significantly reduced virulence in a mouse model of Y. pestis pathogenesis. Our results indicate that the Y. pestis–C. elegans pathogenesis system that is described here can be used to identify and study previously uncharacterized Y. pestis gene products required for virulence in mammalian systems.
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