Repair of Potentially Lethal Damage in Normal Cells and Ataxia Telangiectasia Cells; Consideration of Non-Homologous End-Joining

• KAN'O Momoe

  Department of Radiology, School of Medicine, Keio University Department of Radiology, Graduate School of Medicine, Chiba University

• KAWATA Tetsuya

  Department of Radiology, Graduate School of Medicine, Chiba University

• ITO Hisao

  Department of Radiology, Graduate School of Medicine, Chiba University

• SHIGEMATSU Naoyuki

  Department of Radiology, School of Medicine, Keio University

• LIU Cuihua

  Department of Radiology, Graduate School of Medicine, Chiba University

• UNO Takashi

  Department of Radiology, Graduate School of Medicine, Chiba University

• ISOBE Kouich

  Department of Radiology, Graduate School of Medicine, Chiba University

• KAWAKAMI Hiroyuki

  Department of Radiology, Graduate School of Medicine, Chiba University

• CUCINOTTA Francis

  NASA Lyndon B Johnson Space Center, Radiation Biophysics Laboratory

• GEORGE Kerry

  NASA Lyndon B Johnson Space Center, Radiation Biophysics Laboratory

• KUBO Atsushi

  Department of Radiology, School of Medicine, Keio University

Bibliographic Information

Other Title

• Repair of potentially lethal damage in normal cells and ataxia telangiectasis cells; consideration of non-homologous end-joining

Abstract

When cell lines are held in a quiescent state after irradiation, survival rates are greater than those from cells that are stimulated to grow immediately after irradiation. These differences in survival rates correspond to rates of potentially lethal damage repair. The effects of confluent holding recovery after γ-irradiation were investigated using normal human fibroblasts (AG1522) and ataxia telangiectasia fibroblasts (GM02052). Calyculin-A-induced premature chromosome condensation and fluorescent in situ hybridization were applied to study G2/M chromosomal aberrations. Survival results indicated normal capacity for PLDR in AG1522 cells but that PLDR was extremely compromised in GM02052 cells. The chromosomal aberration frequency decreased when AG1522 cells were allowed to repair for 24-h, whereas 24-hour incubation had little effect on the aberration frequency in GM02052 cells. Since the main mechanism for dsbs repair during G0/G1 phases of the cells cycle involve the non-homologous end-joining (NHEJ) process, our study indicates that for AG1522 cells the NHEJ repair process is more likely to induce accurate chromosome repair under quiescent G0 conditions than proliferating G1 phase, while in GM02052 cells the fidelity of NHEJ is similarly defective at either cell cycle phase. Reduced fidelity of NHEJ may be responsible for PLDR defect and its hyper-radiosensitivity in A-T cells.<br>

Journal

• Journal of Radiation Research

  Journal of Radiation Research 48 (1), 31-38, 2007

  Journal of Radiation Research Editorial Committee

Keywords

• PLDR (potentially lethal damage repair)
• NHEJ (non-homologous end-joining)
• Chromosome aberrations
• FISH (fluorescence in situ hybridization)
• Misrepair

Details

• CRID: 1390001205216199424
• NII Article ID: 110006570514
• NII Book ID: AA00705792
• DOI: 10.1269/jrr.0642
• ISSN: 13499157
• ISSN: 04493060
• NDL BIB ID: 8748517
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I8748517
• Web Site: http://academic.oup.com/jrr/article-pdf/48/1/31/2735803/jrr-48-31.pdf
• Web Site: http://dl.ndl.go.jp/info:ndljp/pid/10918859
• Web Site: https://search.jamas.or.jp/link/ui/2007264187
• Text Lang: en
• Data Source:
  • JaLC
  • NDL
  • Crossref
  • NDL-Digital
  • CiNii Articles
• Abstract License Flag: Disallowed