A missense mutant myostatin causes hyperplasia without hypertrophy in the mouse muscle

Masumi Nishi, Akihiro Yasue, Shinichirou Nishimatu, Tsutomu Nohno, Takashi Yamaoka, Mitsuo Itakura, Keiji Moriyama, Hideyo Ohuchi, Sumihare Noji

Research output: Contribution to journalArticle

74 Citations (Scopus)

Abstract

Myostatin, which is a member of the TGF-β 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.

Original languageEnglish
Pages (from-to)247-251
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume293
Issue number1
DOIs
Publication statusPublished - Jan 1 2002
Externally publishedYes

Keywords

  • Dominant negative
  • GDF-8
  • Hyperplasia
  • Hypertrophy
  • Mouse
  • Myostatin
  • Skeletal muscle
  • Transgenic

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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