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

研究成果: Contribution to journalArticle査読

50 被引用数 (Scopus)

抄録

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.

本文言語英語
ページ(範囲)183-189
ページ数7
ジャーナルComparative Biochemistry and Physiology - A Molecular and Integrative Physiology
155
2
DOI
出版ステータス出版済み - 2 2010

All Science Journal Classification (ASJC) codes

  • 生化学
  • 生理学
  • 分子生物学

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