| Project/Area Number |
14580560
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
環境影響評価(含放射線生物学)
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| Research Institution | IBARAKI UNIVERSITY |
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Principal Investigator |
TAUCHI Hiroshi IBARAKI University, College of Science, Associate Professor, 理学部, 助教授 (70216597)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2003: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2002: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | DNA repair / Homologous recombination / Ionizing radiation / Genome instability- / Gene targeting |
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| Research Abstract |
DNA double-strand break (DSB), which is often induced by ionizing radiation, is the most serious damage in genome. There are at least two pathways which can repair DSBs : non-homologous end joining (NHEJ} and homologous recombination (HR). Nbs1 is the underlying gene for Nijmegen breakage syndrome, and is reported to be a regulator of the both biochemical activity and localization of Rad50/Mre11 complex. We established an Nbs1 knockout cell line by using the chicken DT4o cells in order to investigate the role of the Rad50/Mre11/Nbs1 complex in DSB repair pathway in vertebrate cells. The disruption of Nbs1 reduces gene conversion and sister chromatid exchanges, similar to other HR-deficient mutants, in contrast to their almost normal NHEJ efficiency. A site-specific DSB repair assay using SCneo reporter showed a remarkable reduction of HR events following DSB generation in Nbs1-disrupted cells. The rare recombinants observed in the Nbs1-disrupted cells were frequently found to have aberrant structures, which are possibly arise from an unusual crossover events, suggesting that the Nbs1 complex might be required to process recombination intermediates
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