| Project/Area Number |
02454548
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
放射線5生物学
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| Research Institution | Osaka University |
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Principal Investigator |
SHINAGAWA Hideo Osaka University, Associate Professor Research Institute for Microbial Diseases, 微生物病研究所 (40029799)
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| Co-Investigator(Kenkyū-buntansha) |
IWASAKI Hiroshi Osaka University, Instructor Research Institute for Microbial Diseases, 微生物病研究所, 助手 (60232659)
雨村 光子 大阪大学, 微生物病研究所, 教務職員 (80159467)
牧野 耕三 大阪大学, 微生物病研究所, 助手 (20181620)
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| Project Period (FY) |
1990 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥6,700,000 (Direct Cost: ¥6,700,000)
Fiscal Year 1992: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1991: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1990: ¥3,200,000 (Direct Cost: ¥3,200,000)
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| Keywords | Radiation / Mutagenesis / UmuD protein / MucA protein / DNA polymerase II / polB gene / RuvA, B, C proteins / Holliday structure / DNA修復 / DNA組換え / DNAポリメラーゼ / RuvAタンパク / RuvBタンパク / DNA損傷 / ruvA・B・C遺伝子 / DNAポリメラ-ゼII / SOS反応 / DNAポリメラ-ゼ / umuD,C遺伝子 / mucA,B遺伝子 |
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| Research Abstract |
To elucidate molecular mechanisms of radiation and chemical mutagenesis, we have studiedbiochemical properties of the products of the genes which are known to be involved in mutagenesis in Escherichia coli. The major accomplishments of this project are as follows.
1. RecA protein activated in the DNA-damaged cell promotes cleavage of UnuD and MucA proteins and thereby activates these proteins for mutagenesis.
2. We demonstrated that the polB gene is negatively regulated by LexA repressor (SOS regulation) and that DNA polymerase II encoded by polB is structurally and functionally homologous to replicative DNA polymerases of eukaryotes.
3. We have proved that a RuvA tetramer and RuvB form a stable complex and the complex interacts specifically with the Holliday structure, an intermediate of homologous recombination, and promotes branch migration.
4. We demonstrated biochemically that RuvC protein is a specific endonuclease that resolves the Holliday junction.
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