title: The Caenorhabditis elegans ADAMTS family gene adt-1 is necessary for morphogenesis of the male copulatory organs.
abstract: Remodeling of the extracellular matrix (ECM) is pivotal for various biological processes, including organ morphology and development. The Caenorhabditis elegans male tail has male-specific copulatory organs, the rays and the fan. Ray morphogenesis, which involves a rapid remodeling of the ECM, is an important model of morphogenesis, although its mechanism is poorly understood. ADAMTS (a disintegrin-like and metalloproteinase with thrombospondin type I motifs) is a novel metalloproteinase family that is thought to be an important regulator for ECM remodeling during development and pathological states. We report here that a new C. elegans ADAMTS family gene, adt-1, plays an important regulatory role in ray morphogenesis. Inactivation of the adt-1 gene resulted in morphological changes in the rays as well as the appearance of abnormal protuberances around the rays. In addition, mating ability was remarkably impaired in adt-1 deletion mutant males. Furthermore, we found that the green fluorescent protein reporter driven by the adt-1 promoter was specifically expressed throughout the rays in the male tail. We hypothesize that ADT-1 controls the ray extension process via remodeling of the ECM in the cuticle.
authors.affiliation: Department of Basic and Clinical Oncology, Center for the Development of Molecular Target Drugs, Cancer Research Institute, Kanazawa University, 13-1 Takara-machi, Kanazawa, Ishikawa 920-0934, Japan. kkuno@kenroku.kanazawa-u.ac.jp
authors.forename: Kouji
authors.initials: K
authors.lastname: Kuno
authors.forename: Chie
authors.initials: C
authors.lastname: Baba
authors.forename: Atsuko
authors.initials: A
authors.lastname: Asaka
authors.forename: Chieko
authors.initials: C
authors.lastname: Matsushima
authors.forename: Kouji
authors.initials: K
authors.lastname: Matsushima
authors.forename: Ryuji
authors.initials: R
authors.lastname: Hosono
mesh_terms: D051722:ADAM Proteins; D000071097:ADAMTS1 Protein; D000595:Amino Acid Sequence; D000818:Animals; D030801:Animals, Genetically Modified; D001483:Base Sequence; D017173:Caenorhabditis elegans / Q000737:chemistry* / Q000235:genetics*; D029742:Caenorhabditis elegans Proteins / Q000096:biosynthesis / Q000235:genetics* / Q000502:physiology*; D002417:Cattle; D003360:Cosmids; D019483:Disintegrins / Q000235:genetics*; D005109:Extracellular Matrix / Q000378:metabolism; D017353:Gene Deletion; D017930:Genes, Reporter; D005837:Genitalia, Male / Q000502:physiology*; D049452:Green Fluorescent Proteins; D006801:Humans; D008164:Luminescent Proteins / Q000378:metabolism; D008297:Male; D008666:Metalloendopeptidases / Q000235:genetics*; D051379:Mice; D008957:Models, Genetic; D008969:Molecular Sequence Data; D009154:Mutation; D010641:Phenotype; D020161:Physical Chromosome Mapping; D011401:Promoter Regions, Genetic; D017434:Protein Structure, Tertiary; D011993:Recombinant Fusion Proteins / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017386:Sequence Homology, Amino Acid
chemical_list: C454121:Adt-1 protein, C elegans; D029742:Caenorhabditis elegans Proteins; D019483:Disintegrins; D008164:Luminescent Proteins; D011993:Recombinant Fusion Proteins; D049452:Green Fluorescent Proteins; D051722:ADAM Proteins; D000071097:ADAMTS1 Protein; C103859:ADAMTS1 protein, human; C486323:Adamts1 protein, mouse; D008666:Metalloendopeptidases