Identification of factors interacting with lamin A on the telophase chromosome
| Project/Area Number |
15K07161
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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 |
Genetics/Chromosome dynamics
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| Research Institution | University of Hyogo |
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Principal Investigator |
Hirose Fumiko 兵庫県立大学, 生命理学研究科, 准教授 (60208882)
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| Project Period (FY) |
2015-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | SUMO化 / 核ラミナ / 有糸分裂期 / 脱リン酸化 / クロマチン / ヘテロクロマチン / 分裂期 / 核膜 / ラミンＡ / 翻訳後修飾 / 分裂期終期 |
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| Outline of Final Research Achievements |
I demonstrated evidence that a SUMO-interacting motif (SIM) resided on lamin A polypeptide is required for dephosphorylation of lamin A during telophase and subsequent nuclear lamina formation. I tried to identify factors which allow the recruitment of lamin A to the telophase chromosome and dephosphorylation of the mitotic lamin A phosphorylation. As a result, I found that RepoMan, a regulatory subunit of protein phosphatase 1gamma contributes to lamin A recruitment to telophase chromosomes and dephosphorylation of the mitotic lamin A phosphorylation. Expression of a SUMO2 mutant defective in SUMO-SIM interaction resulted in failure of the lamin A and RepoMan association, along with abrogation of lamin A dephosphorylation and subsequent nuclear lamina formation. These findings strongly suggested that RepoMan/PP1gamma recruits lamin A through SUMO-SIM interaction.
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| Academic Significance and Societal Importance of the Research Achievements |
遺伝物質であるDNAが細胞分裂を経た後も正確に２つの娘細胞に受け継がれる。細胞分裂では染色体の分配と分離を正確に遂行するための仕組みがあり、リン酸化と脱リン酸化のカスケードを介した緻密な制御機構が明らかとなっている。一方で、分裂期の最後に形成される核ラミナと核膜形成のタイミングや場所を調節する仕組みについては不明な点が多かった。本研究では、核ラミナと核膜を再形成させるきっかけが、核ラミナの構成因子であるラミンAたんぱく質の脱リン酸化であり、これを行う酵素が分裂期終期の染色体上にあることを明らかにした。
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Report
(5 results)
Research Products
(14 results)
