| Project/Area Number |
16K08627
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | University of Miyazaki |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
武谷 立 宮崎大学, 医学部, 教授 (50335981)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 心筋 / 細胞骨格 / フォルミンタンパク質 |
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| Outline of Final Research Achievements |
The formin family proteins nucleate and elongate actin filament, thereby functioning in diverse cytoskeletal processes. Fhod3, one of the cardiac formin proteins, plays a crucial role in development and functional maintenance of the heart. On the other hand, the role of Fhod1, a protein closely-related to Fhod3, has still remained elusive. To clarify the physiological role of Fhod1, we generated Fhod1 knockout mice by replacement of exon 1 of the Fhod1 gene with a lacZ reporter gene. Both in histological LacZ staining and in immunoblot analysis, expression level of the Fhod1 protein in the heart was below the lower limit of detection. Fhod1 knockout mice did not show any defects in gross and histological appearance of the heart. Thus, Fhod1 appears to be unnecessary for normal development and function of the mouse heart, even if a marginal amount of Fhod1 is expressed in the heart.
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| Academic Significance and Societal Importance of the Research Achievements |
これまでFhod3が心発生と心機能維持に必須であることを我々は明らかとしてきた。一方、Fhod1は心筋に発現して機能しているという報告もあったが、本研究によってFhod1は心臓において発現が極めて少なく、また発現していたとしても心機能にはほぼ関与していないことを我々は新たに見出した。心臓におけるアクチン核化・重合因子の果たす役割の研究を通して、心筋の収縮力調節機構を正しく理解することで、心不全といった病態機構の原因解明の糸口につながると考えている。
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