title: A reverse genetic analysis of components of the Toll signaling pathway in Caenorhabditis elegans.
abstract: BACKGROUND
  Both animals and plants respond rapidly to pathogens by inducing the expression of defense-related genes. Whether such an inducible system of innate immunity is present in the model nematode Caenorhabditis elegans is currently an open question. Among conserved signaling pathways important for innate immunity, the Toll pathway is the best characterized. In Drosophila, this pathway also has an essential developmental role. C. elegans possesses structural homologs of components of this pathway, and this observation raises the possibility that a Toll pathway might also function in nematodes to trigger defense mechanisms or to control development.
  
  
  RESULTS
  We have generated and characterized deletion mutants for four genes supposed to function in a nematode Toll signaling pathway. These genes are tol-1, trf-1, pik-1, and ikb-1 and are homologous to the Drosophila melanogaster Toll, dTraf, pelle, and cactus genes, respectively. Of these four genes, only tol-1 is required for nematode development. None of them are important for the resistance of C. elegans to a number of pathogens. On the other hand, C. elegans is capable of distinguishing different bacterial species and has a tendency to avoid certain pathogens, including Serratia marcescens. The tol-1 mutants are defective in their avoidance of pathogenic S. marcescens, although other chemosensory behaviors are wild type.
  
  
  CONCLUSIONS
  In C. elegans, tol-1 is important for development and pathogen recognition, as is Toll in Drosophila, but remarkably for the latter rôle, it functions in the context of a behavioral mechanism that keeps worms away from potential danger.
authors.affiliation: Laboratoire de Génétique et Physiologie du Développement, Institut National de la Santé et de la Recherche Médicale/Centre National pour la Recherche Scientifique/Université de la Mediterranée, 13288, Marseille, France.
authors.forename: N
authors.initials: N
authors.lastname: Pujol
authors.forename: E M
authors.initials: EM
authors.lastname: Link
authors.forename: L X
authors.initials: LX
authors.lastname: Liu
authors.forename: C L
authors.initials: CL
authors.lastname: Kurz
authors.forename: G
authors.initials: G
authors.lastname: Alloing
authors.forename: M W
authors.initials: MW
authors.lastname: Tan
authors.forename: K P
authors.initials: KP
authors.lastname: Ray
authors.forename: R
authors.initials: R
authors.lastname: Solari
authors.forename: C D
authors.initials: CD
authors.lastname: Johnson
authors.forename: J J
authors.initials: JJ
authors.lastname: Ewbank
mesh_terms: D000192:Actinomycetales / Q000472:pathogenicity; D000595:Amino Acid Sequence; D000818:Animals; D001203:Ascomycota / Q000472:pathogenicity; D001483:Base Sequence; D001522:Behavior, Animal / Q000502:physiology*; D017173:Caenorhabditis elegans / Q000382:microbiology / Q000502:physiology*; D029742:Caenorhabditis elegans Proteins; D017124:Conserved Sequence; D004268:DNA-Binding Proteins; D029721:Drosophila Proteins; D017238:Genes, Helminth; D005804:Genes, Lethal; D015801:Helminth Proteins / Q000235:genetics / Q000378:metabolism*; D007113:Immunity, Innate; D003904:Mitosporic Fungi / Q000472:pathogenicity; D008969:Molecular Sequence Data; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism*; D010750:Phosphoproteins; D017346:Protein Serine-Threonine Kinases; D011550:Pseudomonas aeruginosa / Q000472:pathogenicity; D017386:Sequence Homology, Amino Acid; D015398:Signal Transduction
chemical_list: D029742:Caenorhabditis elegans Proteins; D004268:DNA-Binding Proteins; D029721:Drosophila Proteins; D015801:Helminth Proteins; D009419:Nerve Tissue Proteins; D010750:Phosphoproteins; C439300:Tol-1 protein, C elegans; C077938:cact protein, Drosophila; C079896:pll protein, Drosophila; D017346:Protein Serine-Threonine Kinases