| Project/Area Number |
15K18799
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Integrative animal science
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| Research Institution | Kanazawa University |
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Principal Investigator |
KAMEI HIROYASU 金沢大学, 自然システム学系, 助教 (00610362)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | ゼブラフィッシュ / 低酸素 / 成長遅滞 / 追いつき成長 / インスリン・インスリン様成長因子シグナル / 神経堤細胞 / 再酸素処理 / ゼブラフィッシュ胚 / インスリン様シグナル |
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| Outline of Final Research Achievements |
Most animals retard growth in response to adverse conditions; however, upon the removal of unfavorable factors, they often show quick growth restoration, which is known as “catch-up” growth. In this study, by using zebrafish embryo model of hypoxia/reoxygenation-induced catch-up growth, I aimed to know how the neural crest cells (NCCs) and insulin/insulin-like growth factor signaling (IIS) play roles in this phenomenon. I found that the viability of NCCs was maintained under hypoxia with the activation of IIS at certain level, and it was seemingly crucial for the survival of these cells during the stunting period. In addition, by next generation sequencing analysis, previously unreported “catch-up growth”-related genes were discovered in this study. These results could be an aid for decoding the mechanism underlying various physiological changes including adult onset disease induced by growth arrest and by subsequent growth restoration at the early stages of animal growth.
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