Disruption of the BLM gene in ATM-null DT40 cells does not exacerbate either phenotype

Toshiyuki Fukao, Philip Chen, Jun Ren, Hideo Kaneko, Gai Xiu Zhang, Masahi Kondo, Ken Ichi Yamamoto, Yasuhiro Furuichi, Shunichi Takeda, Naomi Kondo, Martin F. Lavin

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Bloom syndrome and ataxia-telangiectasia are autosomal recessive human disorders characterized by immunodeficiency, genome instability and predisposition to develop cancer. Recent data reveal that the products of these two genes, BLM and ATM, interact and function together in recognizing abnormal DNA structures. To investigate the function of these two molecules in DNA damage recognition, we generated double knockouts of ATM-/- BLM -/- in the DT40 chicken B-lymphocyte cell line. The double mutant cells were viable and exhibited a variety of characteristics of both ATM -/- and BLM-/- cells. There was no evidence for exacerbation of either phenotype; however, the more extreme radiosensitivity seen in ATM-/- and the elevated sister chromatid exchange seen in BLM-/- cells were retained in the double mutants. These results suggest that ATM and BLM have largely distinct roles in recognizing different forms of damage in DNA, but are also compatible with partially overlapping functions in recognizing breaks in radiation-damaged DNA.

Original languageEnglish
Pages (from-to)1498-1506
Number of pages9
JournalOncogene
Volume23
Issue number8
DOIs
Publication statusPublished - Feb 26 2004
Externally publishedYes

Keywords

  • Ataxia-telangiectasia
  • Bloom syndrome
  • DNA damage
  • DT40 cells
  • Gene disruption

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research

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  • Cite this

    Fukao, T., Chen, P., Ren, J., Kaneko, H., Zhang, G. X., Kondo, M., Yamamoto, K. I., Furuichi, Y., Takeda, S., Kondo, N., & Lavin, M. F. (2004). Disruption of the BLM gene in ATM-null DT40 cells does not exacerbate either phenotype. Oncogene, 23(8), 1498-1506. https://doi.org/10.1038/sj.onc.1207276