Multiple Genes Affect Sensitivity of Caenorhabditis elegans to the Bacterial Pathogen Microbacterium nematophilum

Interactions with bacteria play a major role in immune responses, ecology, and evolution of all animals, but they have been neglected until recently in the case of C. elegans. We report a genetic investigation of the interaction of C. elegans with the nematode-specific pathogen Microbacterium nemato...

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Published in:	Genetics (Austin) Vol. 171; no. 3; pp. 1033 - 1045
Main Authors:	Gravato-Nobre, Maria J, Nicholas, Hannah R, Nijland, Reindert, O'Rourke, Delia, Whittington, Deborah E, Yook, Karen J, Hodgkin, Jonathan
Format:	Journal Article
Language:	English
Published:	United States Genetics Soc America 01-11-2005 Genetics Society of America Copyright © 2005 by the Genetics Society of America
Subjects:	Actinomycetales - pathogenicity Actinomycetales Infections - microbiology Animals Bacteria Caenorhabditis elegans Caenorhabditis elegans - genetics Caenorhabditis elegans - metabolism Caenorhabditis elegans - microbiology Caenorhabditis elegans Proteins - genetics Caenorhabditis elegans Proteins - metabolism Chromosome Mapping Exoribonucleases - genetics Exoribonucleases - metabolism Genetic Markers Genetic Predisposition to Disease Genetics Investigations Lectins - metabolism Male Medical research Microbacterium Mutation Nematoda Nematodes Phenotype
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Summary:	Interactions with bacteria play a major role in immune responses, ecology, and evolution of all animals, but they have been neglected until recently in the case of C. elegans. We report a genetic investigation of the interaction of C. elegans with the nematode-specific pathogen Microbacterium nematophilum, which colonizes the rectum and causes distinctive tail swelling in its host. A total of 121 mutants with altered response to infection were isolated from selections or screens for a bacterially unswollen (Bus) phenotype, using both chemical and transposon mutagenesis. Some of these correspond to known genes, affecting either bacterial adhesion or colonization (srf-2, srf-3, srf-5) or host swelling response (sur-2, egl-5). Most mutants define 15 new genes (bus-1-bus-6, bus-8, bus-10, bus-12-bus-18). The majority of these mutants exhibit little or no rectal infection when challenged with the pathogen and are probably altered in surface properties such that the bacteria can no longer infect worms. A number have corresponding alterations in lectin staining and cuticle fragility. Most of the uninfectable mutants grow better than wild type in the presence of the pathogen, but the sur-2 mutant is hypersensitive, indicating that the tail-swelling response is associated with a specific defense mechanism against this pathogen.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Corresponding author: Genetics Unit, Department of Biochemistry, University of Oxford, South Parks Rd., Oxford OX1 3QU, United Kingdom. E-mail: jonathan.hodgkin@bioch.ox.ac.uk Present address: Department of Genetics, Groningen Biomolecular Sciences and Biotechnology Institute, NL-9751 NN Haren, The Netherlands. Communicating editor: K. Kemphues Present address: School of Molecular and Microbial Biosciences, University of Sydney, Sydney, NSW2006, Australia.
ISSN:	0016-6731 1943-2631 1943-2631
DOI:	10.1534/genetics.105.045716