2005 Fiscal Year Final Research Report Summary
Analysis of molecular mechanism of homologous recombination in eukaryotes
| Project/Area Number |
16370080
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Molecular biology
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| Research Institution | Osaka University |
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Principal Investigator |
SHINOHARA Akira Osaka University, Institute for Protein Research, Professor, 蛋白質研究所, 教授 (00252578)
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| Project Period (FY) |
2004 – 2005
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| Keywords | recombination / DNA repair / meiosis / gonome instability |
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| Research Abstract |
Homologous recombination, an exchange between DNA strands, plays a role in the maintenance of genome stability and the production of genome diversity. While, in mitosis, it is required for the repair of DNA damage, it is for the segregation of homologous chromosome at meiotic division I. Malfunction of the recombination leads cancer and infertility in human. In order to reveal molecular mechanism of the recombination, we constructed a strain in which a single doubles-strand break site are visualized with Green Fluorescent protein. Using the strain, the assembly/ disassembly of proteins are monitored. Our results suggest that proteins involved in recombination form a ternary complex on ssDNA, whose assembly/disassembly is tightly coupled with the biochemical transition of recombination intermediates. In addition, we have been looking for new genes involved in meiotic recombination in order to get insight in the mechanism of the recombination between homologs. We found that two proteins, Mei5 and Sae3, form a complex, which helps assembly of a meiosis-specific RecA homolog, Dmc1 and cooperates with Dmc1 for the recombination. Furthermore, we also found three new genes involved in meiotic recombination (Spo16, Csm4, Ydr015C) and have been analyzing the phenotypes of the mutants to know the function of the proteins in meiotic recombination.
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