| Project/Area Number |
23300160
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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 Metropolitan Institute of Medical Science |
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Principal Investigator |
KIKKAWA Yoshiaki 公益財団法人東京都医学総合研究所, ゲノム医科学研究分野, プロジェクトリーダー (20280787)
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| Co-Investigator(Kenkyū-buntansha) |
SHITARA Hiroshi 公益財団法人東京都医学総合研究所, 基盤技術研究センター, 主任基盤技術研究職員 (90321885)
NOGUCHI Yoshihiro 東京医科歯科大学, 医学部附属病院, 講師 (50282752)
WADA Kenta 東京農業大学, 生物産業学部, 助教 (20508113)
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| Research Collaborator |
SUZUKI Sari 東京農業大学, 大学院生物産業学研究科
MIYASAKA Yuki 新潟大学, 大学院医歯学総合研究科
OBARA Yo 筑波大学, 大学院生命環境科学研究科
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| Project Period (FY) |
2011-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥18,850,000 (Direct Cost: ¥14,500,000、Indirect Cost: ¥4,350,000)
Fiscal Year 2014: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2013: ¥6,110,000 (Direct Cost: ¥4,700,000、Indirect Cost: ¥1,410,000)
Fiscal Year 2012: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2011: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | 遺伝学 / 遺伝子 / ゲノム / 加齢性難聴 / 難聴モデルマウス / QTL / コンソミック系統 / Lrrc30 / カドヘリン / モデルマウス / 近交系マウス / Cadherin23 |
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| Outline of Final Research Achievements |
We performed quantitative trait locus (QTL) linkage analysis and comprehensive gene expression analysis to identify the susceptibility and resistance genes in the onset of age-related hearing loss (AHL) by using mouse models of human AHL. QTL linkage analysis showed that the multiple susceptibility loci on chromosome 5 were involved in early-onset AHL of the DBA/2J mice. QTL linkage analysis also suggested that the hearing loss in NOD/Shi mice developed owing to the effects of the susceptibility loci on chromosomes 1, 5, 6, 9, and 10. Moreover, AHL in the C57BL/6J mice was suppressed by transgenesis of AHL resistance MSM/Ms mice-derived genomic DNA, including the leucine-rich repeat containing 30 gene (Lrrc30) on chromosome 17; the suppression of AHL in C57BL/6J mice was caused by the increased Lrrc30 expression following the transgenesis. These findings on AHL-related loci and genes in mice might be useful in the genetic diagnosis of AHL in humans.
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