Ionizing radiation does not impair the mechanisms controlling genetic stability during T cell receptor gene rearrangement in mice

Serge M. Candéias*, Sylwia Kabacik, Ann Karin Olsen, Dag M. Eide, Dag A. Brede, Simon Bouffler, Christophe Badie

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)

Abstract

Purpose: To determine whether low dose/low dose rate radiation-induced genetic instability may result from radiation-induced inactivation of mechanisms induced by the ATM-dependent DNA damage response checkpoint. To this end, we analysed the faithfulness of T cell receptor (TR) gene rearrangement by V(D)J recombination in DNA from mice exposed to a single dose of X-ray or chronically exposed to low dose rate γ radiation. Materials and methods: Genomic DNA obtained from the blood or the thymus of wild type or Ogg1-deficient mice exposed to low (0.1) or intermediate/high (0.2–1 Gy) doses of radiation either by acute X-rays exposure or protracted exposure to low dose-rate γ-radiation was used to analyse by PCR the presence of illegitimate TR gene rearrangements. Results: Radiation exposure does not increase the onset of TR gene trans-rearrangements in irradiated mice. In mice where it happens, trans-rearrangements remain sporadic events in developing T lymphocytes. Conclusion: We concluded that low dose/low dose rate ionizing radiation (IR) exposure does not lead to widespread inactivation of ATM-dependent mechanisms, and therefore that the mechanisms enforcing genetic stability are not impaired by IR in developing lymphocytes and lymphocyte progenitors, including BM-derived hematopoietic stem cells, in low dose/low dose rate exposed mice.

Original languageEnglish
Pages (from-to)357-365
Number of pages9
JournalInternational Journal of Radiation Biology
Volume94
Issue number4
DOIs
Publication statusPublished - 7 Mar 2018

Bibliographical note

Publisher Copyright:
© 2018, Copyright © 2018 Taylor & Francis Group LLC.

Keywords

  • ATM
  • DNA damage response
  • T cell receptor genes
  • V(D)J recombination
  • genetic instability
  • low dose/low dose rate radiation
  • trans-rearrangements

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