Determination of a role for autophagy in suppression of genome instability caused by replication stress
| Project/Area Number |
15H05601
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Genetics/Chromosome dynamics
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| Research Institution | Nagasaki University (2017)
Osaka University (2015-2016) |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥23,400,000 (Direct Cost: ¥18,000,000、Indirect Cost: ¥5,400,000)
Fiscal Year 2017: ¥8,190,000 (Direct Cost: ¥6,300,000、Indirect Cost: ¥1,890,000)
Fiscal Year 2016: ¥8,190,000 (Direct Cost: ¥6,300,000、Indirect Cost: ¥1,890,000)
Fiscal Year 2015: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
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| Keywords | オートファジー / 複製ストレス / ゲノム安定性 / がん / DNA複製ストレス / ゲノム安定性の維持 / タンパク質凝集体 / ガン |
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| Outline of Final Research Achievements |
Despite of redundant DNA repair systems, cells suffer tumor-causing gross chromosomal rearrangements caused by replication stress. Although recent evidence suggests that replication stress response suppresses these aberrations, the mechanism how replication stress promotes tumorigenesis in vivo is still under debate. Here we show that autophagy, intracellular bulk degradation system, protects cells from genome instability caused by replication stress. Compromise in basal autophagy results in deregulation of DNA repair systems and increase in chromosomal instability, which stem from deregulated pathway choice. Altogether, we propose that replication stress response and autophagy cooperatively facilitate chromosomal integrity during genome duplication.
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Report
(4 results)
Research Products
(4 results)
