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BER Research Highlights

Cell-Cycle Checkpoint Control Exhibits Nonlinear Behavior at Low Radiation Doses
Published: June 01, 2012
Posted: August 20, 2012

When cells are exposed to a radiation dose large enough to cause chromosome aberrations, they are normally arrested at the G2/M checkpoint, which facilitates DNA repair. New research confirms an activation threshold for the G2/M cell-cycle checkpoint, hinting at two separate radiation response mechanisms that act below and above this threshold. When arrest kinetics were monitored in mouse embryo fibroblasts over a range of low doses and time, no significant checkpoint activation was observed at doses below 100 mGy. Parallel measure¬ments done with cells haplo-insufficient for one or more radioresistance genes showed similar checkpoint activation kinetics. This is in contrast to previous work showing that haplo-insufficiency for several radioresistance genes imparts intermediate phenotypes for endpoints including apoptosis, transformation, and survival. These findings suggest that checkpoint control does not contribute toward these intermediate phenotypes and that different biological processes can be activated at high doses compared to low doses. The journal selected the first author, Erik Young, for its Editors' Award to a Radiation Research Society Scholar-in-Training as the best paper of the last year.

Reference: Young, E. F., L. B. Smilenov, H. B., Lieberman, and E. J. Hall. 2012. "Combined Haplo-Insufficiency and Genetic Control of the G2/M Checkpoint in Irradiated Cells," Radiation Research 177(6), 743-750. DOI: 10.1667/RR2875.1. (Reference link)

Contact: Noelle Metting, SC-23.2, (301) 903-8309
Topic Areas:

  • Cross-Cutting: Lectures, Awards, and Recognition
  • Legacy: Low Dose Radiation, Radiobiology

Division: SC-33.2 Biological Systems Science Division, BER


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