Mechanism of reactivation of replication forks stalled by DNA damage
| Project/Area Number |
24710059
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Risk sciences of radiation/Chemicals
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| Research Institution | Hiroshima University |
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Principal Investigator |
MIYAMOTO Mayumi 広島大学, 理学(系)研究科(研究院), 特任助教 (10457278)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | DNA複製 / 相同組換え |
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| Research Abstract |
DNA replication forks are stalled when they encounter genome damage. However, it has not been fully elucidated how stalled replication forks are reactivated and complete DNA synthesis in higher eukaryotes. In the present study we analyzed the sensitivity of DNA repair mutants to various DNA-protein cross-link (DPC) agents and accumulation of DNA double-strand breaks (DSB). Cells deficient in homologous recombination (HR) were hypersensitive to DPC-inducing agents. The HR-deficient but not wild type cells accumulated DSBs upon treatment with DPC-inducing agents. These results suggest that replication forks that are stalled by DPCs undergo breakage and that the resulting DSB ends are processed by HR to resume DNA replication.
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Report
(3 results)
Research Products
(7 results)
