title: MyD88-deficient Hydra reveal an ancient function of TLR signaling in sensing bacterial colonizers.
abstract: Toll-like receptor (TLR) signaling is one of the most important signaling cascades of the innate immune system of vertebrates. Studies in invertebrates have focused on the fruit fly Drosophila melanogaster and the nematode Caenorhabditis elegans, and there is little information regarding the evolutionary origin and ancestral function of TLR signaling. In Drosophila, members of the Toll-like receptor family are involved in both embryonic development and innate immunity. In C. elegans, a clear immune function of the TLR homolog TOL-1 is controversial and central components of vertebrate TLR signaling including the key adapter protein myeloid differentiation primary response gene 88 (MyD88) and the transcription factor NF-κB are not present. In basal metazoans such as the cnidarians Hydra magnipapillata and Nematostella vectensis, all components of the vertebrate TLR signaling cascade are present, but their role in immunity is unknown. Here, we use a MyD88 loss-of-function approach in Hydra to demonstrate that recognition of bacteria is an ancestral function of TLR signaling and that this process contributes to both host-mediated recolonization by commensal bacteria as well as to defense against bacterial pathogens.
authors.affiliation: Zoological Institute,  Christian Albrechts University, 24098 Kiel,  Germany.
authors.forename: Sören
authors.initials: S
authors.lastname: Franzenburg
authors.forename: Sebastian
authors.initials: S
authors.lastname: Fraune
authors.forename: Sven
authors.initials: S
authors.lastname: Künzel
authors.forename: John F
authors.initials: JF
authors.lastname: Baines
authors.forename: Tomislav
authors.initials: T
authors.lastname: Domazet-Loso
authors.forename: Thomas C G
authors.initials: TC
authors.lastname: Bosch
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D001483:Base Sequence; D015169:Colony Count, Microbial; D004198:Disease Susceptibility / Q000276:immunology / Q000382:microbiology; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation / Q000187:drug effects; D055785:Gene Knockdown Techniques; D006829:Hydra / Q000187:drug effects / Q000235:genetics / Q000276:immunology* / Q000382:microbiology*; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D053594:Myeloid Differentiation Factor 88 / Q000172:deficiency* / Q000378:metabolism; D020411:Oligonucleotide Array Sequence Analysis; D010766:Phosphorylation / Q000187:drug effects; D011552:Pseudomonas Infections / Q000276:immunology / Q000382:microbiology; D011550:Pseudomonas aeruginosa / Q000187:drug effects / Q000254:growth & development*; D012336:RNA, Ribosomal, 16S / Q000235:genetics; D017423:Sequence Analysis, RNA; D015398:Signal Transduction / Q000187:drug effects / Q000276:immunology*; D051193:Toll-Like Receptors / Q000187:drug effects / Q000276:immunology*
chemical_list: D000900:Anti-Bacterial Agents; D053594:Myeloid Differentiation Factor 88; D012336:RNA, Ribosomal, 16S; D051193:Toll-Like Receptors; D048031:JNK Mitogen-Activated Protein Kinases