| Project/Area Number |
21710059
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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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 |
NAKANO Toshiaki Hiroshima University, 大学院・理学研究科, 助教 (10526122)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2009: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 修復 / 複製 / 転写 / DNA-タンパク質クロスリンク / DNA-タンパク質クロスリンク損傷 / DNA複製 / DnaB |
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| Research Abstract |
DNA-protein crosslinks (DPCs) are extremely bulky genomic lesions and are not efficiently repaired by nucleotide excision repair, suggesting that DPCs will exert detrimental effects on DNA replication and transcription in cells. In this study, we have prepared model DNA substrates containing site-specific DPCs and assessed their effects on DNA replication and transcription in vitro. DPCs on the lagging strand inhibited the progression of DnaB, the replicative helicase of E. coif, in a DPC size-dependent manner. Conversely DPCs on the leading strand had no effects on the progression of DnaB. We also have prepared DNA templates containing DPCs for in vitro transcriptions studies with T7 RNA polymerase. We are currently assessing the effects of DPCs in transcribed and nontranscribed strands on transcription.
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