Shinichiro Nishimatsu    Department   Kawasaki Medical School  Kawasaki Medical School, Department of Natural Sciences,    Position   Professor
Article types	原著
Language	English
Peer review	Peer reviewed
Title	A missense mutant myostatin causes hyperplasia without hypertrophy in the mouse muscle.
Journal	Formal name：Biochemical and biophysical research communications Abbreviation：Biochem Biophys Res Commun ISSN code：0006291X/10902104
Volume, Issue, Page	293(1),pp.247-251
Author and coauthor	Nishi Masumi, Yasue Akihiro, Nishimatu Shinichirou, Nohno Tsutomu, Yamaoka Takashi, Itakura Mitsuo, Moriyama Keiji, Ohuchi Hideyo, Noji Sumihare
Publication date	2002/04
Summary	Myostatin, which is a member of the TGF-beta superfamily, is a negative regulator of skeletal muscle formation. Double-muscled Piedmontese cattle have a C313Y mutation in myostatin and show increased skeletal muscle mass which resulted from an increase of myofiber number (hyperplasia) without that of myofiber size (hypertrophy). To examine whether this mutation in myostatin gene affects muscle development in a dominant negative manner, we generated transgenic mice overexpressing the mutated gene. The transgenic mice exhibited dramatic increases in the skeletal muscle mass resulting from hyperplasia without hypertrophy. In contrast, it has been reported that a myostatin mutated at its cleavage site produces hypertrophy without hyperplasia in the muscle. Thus, these results suggest that (1) the myostatin containing the missense mutation exhibits a dominant negative activity and that (2) there are two types in the dominant negative form of myostatin, causing either hypertrophy or hyperplasia.
DOI	10.1016/S0006-291X(02)00209-7
Document No.	12054591