Host: The Japan Radiation Research Society
Co-host: Asian Association for Radiation Research
It has been generally accepted that LDRE results from the SLD repair. As the dose rate is lowered and the treatment time protracted, more and more SLD can be repaired during the exposure. Recently we found that SLD recovery is due to DSB repair mediated by HR. To study the molecular mechanism of LDRE, we analyzed the knock-out mutants KU70-/-, RAD54-/-, and KU70-/-/RAD54-/- of the chicken B-cell line, DT40. Rad54 participates in the HR repair of DSBs in S and G2 phase, while Ku proteins are involved in NHEJ and work in whole cell cycle. Survival enhancement by LDR irradiation was observed in parent DT40 and RAD54-/- cells but not in NHEJ deficient KU70-/- and KU70-/-/RAD54-/- cells. In the LDRE, NHEJ pathway was more important than HR pathway. This suggests that LDRE are not directly attributable to the SLD repair because the SLD repair results from the HR pathway of DSBs in S and G2 phase. Under continuous LDR irradiation, dividing NHEJ-deficient cells will be irradiated and killed in G1 phase. NHEJ pathway plays an important role in LDRE. We studied further the effect of low dose-rate irradiation using the NHEJ deficient KU70-/- and KU70-/-/RAD54-/- cells.
