Abstract
It has been generally accepted that LDRE results from the SLD repair. 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. Survival enhancement by LDR irradiation was observed in parent DT40 and RAD54-/- cells but not in NHEJ deficient KU70-/- and KU70-/-/RAD54-/- cells. Under continuous LDR irradiation, dividing NHEJ-deficient cells will be irradiated and killed in G1 phase. In the LDRE, NHEJ pathway was more important than HR pathway. We studied further the effect of low dose-rate irradiation using the deficient KU70-/- and KU70-/-/53BP1-/- cells since 53BP1 is reported to play a role in new NHEJ repair. KU70-/- cells survived well under 0.5 Gy/day compared to 1.0 Gy/day dose rate irradiation. KU70-/-/53BP1-/- cells were sensitive than KU70-/- cells under 0.5Gy/day dose rate irradiation. This suggests that 53BP1 dependent NHEJ is independent Ku/DNA-PK NHEJ and also that both NHEJ pathway play a role in the LDRE.
