Abstract
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 repair 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, while Ku proteins are involved in NHEJ. 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. Under continuous LDR irradiation, dividing chicken cells can progress through the cell cycle. Since NHEJ-deficient cells will be killed in G1 phase, NHEJ pathway plays an important role in LDRE. [J Radiat Res 44:375-376 (2003)]
