Overexpression of the dominant-negative form of myostatin results in doubling of muscle-fiber number in transgenic medaka (Oryzias latipes)

Etsuko Sawatari, Ryoko Seki, Tomoko Adachi, Hisashi Hashimoto, Susumu Uji, Yuko Wakamatsu, Takahiro Nakata, Masato Kinoshita

Research output: Contribution to journalArticle

46 Citations (Scopus)

Abstract

In addition to altering the phenotypes of gene-modified animals, transgenesis also has the potential to facilitate access to the various mechanisms underlying the development and functioning of specific phenotypes and genes, respectively. Myostatin (MSTN) is implicated in double-muscling when mutated in mammals, indicating that MSTN is a negative regulator of skeletal muscle formation. In order to elucidate the role of an MSTN equivalent in fish muscle formation, we created a transgenic medaka strain that expresses dominant-negative MSTN exclusively in skeletal muscle, d-rR-Tg(OlMA1-C315Y-MSTN-hrGFPII-FLAG). The transgenic fish exhibited increased production of skeletal muscle fibers at the adult stage (hyperplasia), although gross muscle mass was not altered. During embryogenesis, ectopic accumulation and misalignment of muscle fibers, possibly due to muscle-fiber hypertrophy, were observed in the transgenic medaka. Our findings suggest that MSTN function is required for regulating the appropriate growth of skeletal muscle in medaka. Unlike in mammals, MSTN loss-of-function failed to induce double-muscling in medaka, despite the highly conserved nature of MSTN function among taxa.

Original languageEnglish
Pages (from-to)183-189
Number of pages7
JournalComparative Biochemistry and Physiology - A Molecular and Integrative Physiology
Volume155
Issue number2
DOIs
Publication statusPublished - Feb 2010

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Physiology
  • Molecular Biology

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