| Project/Area Number |
20570169
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Molecular biology
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| Research Institution | National Institute of Genetics |
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Principal Investigator |
YAMAO Fumiaki National Institute of Genetics, 分子遺伝研究系, 教授 (10158074)
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| Co-Investigator(Kenkyū-buntansha) |
TSUTSUI Yasuhiro 東京工業大学, 大学院・生命理工学研究科, 助教 (00390625)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 染色体機能 / セントロメア / 翻訳後修飾 / 染色体複製 / 遺伝学 / 遺伝子 / 核酸 / タンパク質 / ヒストン / CEN-A / DNA複製 / ヘテロクロマチン / 脱アセチル化 |
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| Research Abstract |
Specialized chromatin exists at centromeres and must be precisely transmitted during DNA replication. The mechanisms involved in the propagation of these structures remain elusive. Fission yeast centromeres are composed of two chromatin domains : the central CENP-A(Cnp1) kinetochore domain and flanking heterochromatin domains. We showed that fission yeast Mcl1, a DNA polymerase alpha (Pol alpha) accessory protein, is critical for maintenance of centromeric chromatin. In a screen for mutants that alleviate both central domain and outer repeat silencing, we isolated several cos mutants, of which cos1 is allelic to mcl1. The mcl1-101 mutation caused reduced CENP-A(Cnp1) in the central domain and an aberrant increase in histone acetylation in both domains. These phenotypes were also observed in a mutant of swi7(+), which encodes a catalytic subunit of Pol alpha. Mcl1 formed S-phase-specific nuclear foci, which colocalized with those of PCNA and Pol alpha. These results suggest that Mcl1 and Pol alpha are required for propagation of centromere chromatin structures during DNA replication.
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