title: Multiple genes affect sensitivity of Caenorhabditis elegans to the bacterial pathogen Microbacterium nematophilum.
abstract: 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.
authors.affiliation: Genetics Unit, Department of Biochemistry, University of Oxford, Oxford OX1 3QU, United Kingdom.
authors.forename: Maria J
authors.initials: MJ
authors.lastname: Gravato-Nobre
authors.forename: Hannah R
authors.initials: HR
authors.lastname: Nicholas
authors.forename: Reindert
authors.initials: R
authors.lastname: Nijland
authors.forename: Delia
authors.initials: D
authors.lastname: O'Rourke
authors.forename: Deborah E
authors.initials: DE
authors.lastname: Whittington
authors.forename: Karen J
authors.initials: KJ
authors.lastname: Yook
authors.forename: Jonathan
authors.initials: J
authors.lastname: Hodgkin
mesh_terms: D000192:Actinomycetales / Q000472:pathogenicity; D000193:Actinomycetales Infections / Q000382:microbiology; D000818:Animals; D017173:Caenorhabditis elegans / Q000235:genetics* / Q000378:metabolism / Q000382:microbiology*; D029742:Caenorhabditis elegans Proteins / Q000235:genetics / Q000378:metabolism; D002874:Chromosome Mapping; D005095:Exoribonucleases / Q000235:genetics / Q000378:metabolism; D005819:Genetic Markers; D020022:Genetic Predisposition to Disease; D037102:Lectins / Q000378:metabolism; D008297:Male; D009154:Mutation; D010641:Phenotype
chemical_list: D029742:Caenorhabditis elegans Proteins; D005819:Genetic Markers; D037102:Lectins; D005095:Exoribonucleases; C496085:MUT-7 protein, C elegans