| Project/Area Number |
06404002
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
遺伝
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| Research Institution | Osaka University |
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Principal Investigator |
SHINAGAWA Hideo Res.Inst.Microbial Diseases, Osaka Univ.Professor, 微生物病研究所, 教授 (40029799)
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| Co-Investigator(Kenkyū-buntansha) |
IWASAKI Hiroshi Res.Inst.Microbial Diseases, Osaka Univ.Research Associate, 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)
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| Project Period (FY) |
1994 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥24,600,000 (Direct Cost: ¥24,600,000)
Fiscal Year 1996: ¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 1995: ¥6,200,000 (Direct Cost: ¥6,200,000)
Fiscal Year 1994: ¥14,800,000 (Direct Cost: ¥14,800,000)
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| Keywords | DNA recombination / DNA repair / Holliday junction / Mutant / RecG protein / RuvA protein / RuvB protein / RuvC protein / RuvCエンドヌクレアーゼ / RuvGタンパク質 / RuvCタンパク / エンドヌクレアーゼ / X線結晶回折 / 染色体 |
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| Research Abstract |
We studied reaction mechanisms and functions of RuvA and RuvB protein complex and RecG protein which drives branch migration of Holliday junctions and RuvC protein which endonucleolytically resolves Holliday junctions.
1.We discovered that RecG protein has a unique function to resolve the R-loops formed at the replication origin and negatively regulate the initiation of replication.
2.We studied the substrate specificity of RuvC resolvase with various synthetic Holliday junctions and found that the existence of thymine residue at or near crossover point is important but the sequence homology at the junction is not important for the cleavage.
3.We cloned and analyzed the ruvA,ruvB and ruvC genes of Pseudomonas aeruginosa and found that although the arrangement of the genes are different from that of the Escherichia coli genes, they possess the similar functions.
4.We cloned, expressed the Thermus thermophilus ruvB gene and characterized the RuvB protein.
5.We studied the morphology of ruv mutants and recG mutants and found that the abortive recombination in these mutants inhibit the chromosome nondisjunction.
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