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Cell cycle dependent DNA break increase in ataxia telangiectasia lymphoblasts after radiation exposure
  1. B Humar1,
  2. H Müller2,
  3. R J Scott3
  1. 1Research Group Human Genetics, Department of Research, University Clinics, CH-4031 Basel, Switzerland
  2. 2Department of Medical Genetics, University Children's Hospital, CH-4058 Basel, Switzerland
  3. 3Discipline of Medical Genetics, Faculty of Medicine and Health Sciences, University of Newcastle, Callaghan, NSW 2308, Australia
  1. Professor Scott rscott{at}


The most striking feature of ataxia telangiectasia (AT) cells is their profound sensitivity to ionising radiation. A deficiency in the rejoining of radiation induced DNA breaks has been suggested to be responsible for AT radiosensitivity; however, the existing literature is controversial. A subpopulation, which is present in irradiated AT lymphoblasts, but rarely in controls, has been reported previously. The cells that make up this subpopulation harbour highly fragmented DNA and are responsible for the overall increase in DNA breaks soon after irradiation in AT lymphoblasts. This study examines the influence of the cell cycle on the highly damaged subpopulation. The frequency of highly damaged cells was highest when AT lymphoblasts were irradiated during the G2/M phase. In contrast, AT lymphoblasts irradiated during the G0/G1 phase displayed a frequency similar to control cells. Thus, only G2/M and to some extent S phase cells contribute to an increased DNA break number in AT lymphoblasts early after irradiation. These findings might explain several inconsistencies reported in the literature.

  • ataxia telangiectasia
  • radiation
  • DNA breaks
  • cell cycle

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