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Originally published In Press as doi:10.1074/jbc.M200144200 on January 16, 2002

J. Biol. Chem., Vol. 277, Issue 14, 12228-12236, April 5, 2002
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The Caenorhabditis elegans ADAMTS Family Gene adt-1 Is Necessary for Morphogenesis of the Male Copulatory Organs*

Kouji KunoDagger **§, Chie BabaDagger , Atsuko AsakaDagger , Chieko Matsushima, Kouji Matsushima||, and Ryuji Hosono

From the Dagger  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, the  Department of Physical Information, Faculty of Medicine, Kanazawa University, 5-11-80 Kodatsuno, Kanazawa, Ishikawa 920-0942, Japan, and the || Department of Molecular Preventive Medicine, School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113, Japan

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.


* This work was supported by a grant-in-aid for scientific research from the Ministry of Education, Science, and Culture of Japan.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ To whom correspondence should be addressed. Tel.: 81-76-265-2722; Fax: 81-76-234-4519; E-mail: kkuno@kenroku.kanazawa-u.ac.jp.


Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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