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Molecular and Cellular Biology, January 2003, p. 55-61, Vol. 23, No. 1
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.1.55-61.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Phenotypic Analysis of Meltrin {alpha} (ADAM12)-Deficient Mice: Involvement of Meltrin {alpha} in Adipogenesis and Myogenesis

Tomohiro Kurisaki,1 Aki Masuda,1 Katsuko Sudo,2 Junko Sakagami,2 Shigeki Higashiyama,3 Yoichi Matsuda,4,5 Akira Nagabukuro,5 Atsushi Tsuji,5 Yoichi Nabeshima,6 Masahide Asano,7 Yoichiro Iwakura,2 and Atsuko Sehara-Fujisawa1*

Field of Growth Regulation, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507,1 Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo 108-8639,2 Department of Medical Biochemistry, Ehime University School of Medicine, Ehime 791-0295,3 Laboratory of Animal Cytogenetics, Center for Advanced Science and Technology, Hokkaido University, Sapporo 060-0810,4 Laboratory of Animal Genetics, Graduate School of Bioagricultural Science, Nagoya University, Chikusa-ku, Nagoya 464-8601,5 Department of Pathology and Tumor Biology, Kyoto University Graduate School of Medicine, Kyoto 606-8501,6 Institute for Experimental Animals, School of Medicine, Kanazawa University, Kanazawa 920-8640, Japan7

Received 29 May 2002/ Returned for modification 28 August 2002/ Accepted 7 October 2002

Meltrin {alpha} (ADAM12) is a metalloprotease-disintegrin whose specific expression patterns during development suggest that it is involved in myogenesis and the development of other organs. To determine the roles Meltrin {alpha} plays in vivo, we generated Meltrin {alpha}-deficient mice by gene targeting. Although the number of homozygous embryos are close to the expected Mendelian ratio at embryonic days 17 to 18, ca. 30% of the null pups born die before weaning, mostly within 1 week of birth. The viable homozygous mutants appear normal and are fertile. Most of the muscles in the homozygous mutants appear normal, and regeneration in experimentally damaged skeletal muscle is unimpeded. In some Meltrin {alpha}-deficient pups, the interscapular brown adipose tissue is reduced, although the penetrance of this phenotype is low. Impaired formation of the neck and interscapular muscles is also seen in some homozygotes. These observations suggest Meltrin {alpha} may be involved in regulating adipogenesis and myogenesis through a linked developmental pathway. Heparin-binding epidermal growth factor-like growth factor (HB-EGF) is a candidate substrate of Meltrin {alpha}, and we found that TPA (12-O-tetradecanoylphorbol-13-acetate)-induced ectodomain shedding of HB-EGF is markedly reduced in embryonic fibroblasts prepared from Meltrin {alpha}-deficient mice. We also report here the chromosomal locations of Meltrin {alpha} in the mouse and rat.

* Corresponding author. Mailing address: Field of Growth Regulation, Institute for Frontier Medical Sciences, Kyoto University, Kyoto, 606-8507, Japan. Phone: 81-75-751-3826. Fax: 81-75-751-4642. E-mail: asehara{at}frontier.kyoto-u.ac.jp.

Molecular and Cellular Biology, January 2003, p. 55-61, Vol. 23, No. 1
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.1.55-61.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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