2017 Fiscal Year Final Research Report
Regulatory mechanisms of replication origin activation.
Project/Area Number |
15H04330
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Molecular biology
|
Research Institution | Osaka University |
Principal Investigator |
|
Project Period (FY) |
2015-04-01 – 2018-03-31
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Keywords | テロメア / 複製開始 / 細胞周期 / 分裂酵母 / shelterin / Taz1 / Rif1 / PP1 |
Outline of Final Research Achievements |
We found that the N-terminal 119 amino acid region of fission yeast Sld3 interacts each other and stabilizes Sld3 protein in the cells. Thus, it contributes to formation of bidirectional replication forks in replication initiation. On the other hand, the Taz1-dependent late replication origins that are visualized by lacO/LacI-GFP are localized at the nuclear periphery throughout the interphase, and associate with the telomeres specifically in the G1/S phase. The shelterin components play roles in tethering of the internal replication origins to the telomeres. The telomeric association of the replication origins causes suppression of early initiation by Rif1 and PP1 that are enriched at the telomeres.
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Free Research Field |
分子遺伝学
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