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

Authors
Journal
Biochemical and Biophysical Research Communications
0006-291X
Publisher
Elsevier
Publication Date
Volume
293
Issue
1
Identifiers
DOI: 10.1016/s0006-291x(02)00209-7
Keywords
  • Mouse
  • Transgenic
  • Myostatin
  • Gdf-8
  • Skeletal Muscle
  • Dominant Negative
  • Hypertrophy
  • Hyperplasia

Abstract

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.

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