Studies on molecular mechanisms that enable high regenerative and growth potential of fish muscle
| Project/Area Number |
26292112
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Aquatic life science
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥16,380,000 (Direct Cost: ¥12,600,000、Indirect Cost: ¥3,780,000)
Fiscal Year 2016: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2014: ¥7,800,000 (Direct Cost: ¥6,000,000、Indirect Cost: ¥1,800,000)
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| Keywords | 筋肉 / 魚 / 終生成長 / 老化 / 魚類 / 再生 / 水産学 / 再生・成長 / 成長 / ゼブラフィッシュ / 筋衛星細胞 / 筋成長 / ミオシン重鎖 / プロモーター / 転写因子 |
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| Outline of Final Research Achievements |
In human, muscle strength declines as aging. This is called as sarcopenia, a decrease in muscle mass and a reduction in regenerative ability associated with aging. On the other hand, in fish, the number of muscle fibers is increased throughout lifespan and regenerative ability is maintained high. Such 'indeterminate growth' of fish is important in understanding fish growth and mammalian sarcopenia, its molecular mechanism is unknown. We focused on a torafugu gene which is expressed in neonatal muscle fibers. In vivo reporter assay of the gene revealed that a NFAT has a significant role in the indeterminate growth. Transcriptome analysis also showed age-related reduction of MSTN/GDF11 and TOR signal in zebrafish muscle. TOR activation in zebrafish caused accerelated aging in muscle. Our results indicate that senescence suppression by TOR signal and maintenance of muscle stem cell by NFAT and MSTN/GDF11 signal are the molecular basis of the indeterminate growth of fish muscle.
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Report
(4 results)
Research Products
(18 results)
