Identification of a causal gene for QTL affecting overweight and resistance to obesity discovered from a gene pool of wild mice
| Project/Area Number |
16H04680
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Laboratory animal science
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| Research Institution | Nagoya University |
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Principal Investigator |
Ishikawa Akira 名古屋大学, 生命農学研究科, 准教授 (20211724)
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| Project Period (FY) |
2016-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥17,550,000 (Direct Cost: ¥13,500,000、Indirect Cost: ¥4,050,000)
Fiscal Year 2019: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2018: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2017: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2016: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
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| Keywords | マウス / QTL / 肥満 / 体重 / ＱＴＬ |
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| Outline of Final Research Achievements |
Overweight and obesity in humans are main risk factors for lifestyle diseases which are controlled by multiple genetic loci (QTLs: quantitative trait loci) and environment. To identify causal genes for the QTLs remains challenging. In this study, by using new analytical approaches, I first identified the Ly75 (lymphocyte antigen 75) gene for an immune system as a causal gene for a QTL affecting resistance to obesity that was previously discovered from a gene pool of wild mice.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究成果は、肥満に関わるQTLの責任遺伝子を同定した数少ない成功例の一つと位置付けることができる。Ly75遺伝子の脂質代謝に関わる役割は全く報告されていないので、本研究成果は、肥満生物学に新しい知見を提供するものと期待できる。また、本研究成果は、ヒトでは、万病の元である肥満を克服するためのゲノム医療への応用が期待できる。さらに、家畜では、家畜の健康改善と畜産物の生産性の向上のためのゲノム育種への応用が期待できる。
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Report
(5 results)
Research Products
(13 results)
