| Project/Area Number |
17H03569
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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 | Tokyo University of Agriculture (2018-2019)
Kyoto University (2017) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
金子 武人 岩手大学, 理工学部, 准教授 (30332878)
須山 幹太 九州大学, 生体防御医学研究所, 教授 (70452365)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥18,720,000 (Direct Cost: ¥14,400,000、Indirect Cost: ¥4,320,000)
Fiscal Year 2019: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2018: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2017: ¥9,490,000 (Direct Cost: ¥7,300,000、Indirect Cost: ¥2,190,000)
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| Keywords | アトピー性皮膚炎 / ラット / QTL解析 / SNP / SSLP / 連鎖解析 / 炎症 / 疾患モデル / ゲノム編集 / 遺伝学 / ゲノム |
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| Outline of Final Research Achievements |
Kyoto Fancy Rat Stock 4 (KFRS4) rats spontaneously developed dermatitis that accompanied an elevation of IgE and scratching behavior. The dermatitis was evidently suppressed by topical application of betamethasone. In addition, KFRS4 rats exhibit skin barrier dysfunction. Thus, the KFRS4 rat is a good model of the atopic dermatitis. Here, we performed quantitative trait locus (QTL) analysis of the onset and severity of the dermatitis in KFRS4 rats. We produced 308 (KFRS4 × PVG)F2 intercross progeny and determined the onset and severity of dermatitis of them. We determined genotypes for 86 SSLP markers and performed QTL analysis with the R/qtl program. We found significant linkage relationships between two SSLP markers with the onset and severity, respectively. Both SSLP makers located on chromosome 17 and mapped within a 3cM-region. Thus, we considered that a QTL that included the two markers influenced the onset and severity.
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| Academic Significance and Societal Importance of the Research Achievements |
アトピー性皮膚炎の優れたモデル動物であるKFRS4ラットの皮膚炎発症に係る遺伝子座を見出した。この遺伝子座には、Th2細胞分化を制御する転写因子Gata3遺伝子が存在しており、Gata3 遺伝子がアトピー性皮膚炎に係る可能性が示唆された。今後、コンジェニック系統や詳細な遺伝子発現解析を行うことで、アトピー性皮膚炎の原因遺伝子の同定が期待される。これにより、多くの人が苦しんでいるアトピー性皮膚炎に対する新たな治療法、予防法が開発されることが期待される。
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