| Project/Area Number |
11680545
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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 | KYOTO UNIVERSITY |
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Principal Investigator |
IWAI Yuko kyoto University, Graduate School of Biostudies, Assistant, 生命科学研究科, 助手 (10281726)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 2000: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1999: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | Ataxia telangiectasia / Nijmegenbreakage syndrome / Ataxia-telangiectasia-like disorder / MRE11 / DT40 / homologousre combination / telomere / chromosomal aberrations / 毛細血管拡張性失調症類似症 / 毛細血管拡張失調症 / ネイミーヘン症 |
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| Research Abstract |
Ataxia telangiectasia (A-T) and Nijmegen breakage syndrome (NBS) are the autosomal reccessive disorders associated with frequent chromosomal aberration and predisposition to cancer. ATM and NBS (Nibrin) have been identified as the gene products deficient in A-T and NBS, respectively. The cellular features of the related disease, ataxia-telangiectasia-like disorder (ATLD) shows similar to those seen in A-T as well as NBS and results from MRE11 mutations. We have generated the conditional MRE11 deficient cells using a hyper-recombinogenic chicken B cell line, DT40 and investigated the function of Mre11. Vertebrate Mre11 is essential. Mre11 deficient DT40 cells accumulate chromosome breaks and die upon Mre11 repression, showing frequent centrosome amplification. Mre11 deficiency also causes increased radiosensitivity and strongly reduced targeted integration frequencies. Mre11 is, therefore, crucial for HR and essential in mitosis through its role in chromosome maintenance by recombinational repair. We also observed the tendency of elongated G-strand overhang in Mre11 deficient cells, suggesting that MRE11 might be involved in the maintenance of telomere structure.
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