抄録
Eukaryotic cells have at least two major pathways to repair DSBs, i.e., non-homologous end joining (NHEJ) and homologous recombination (HR). In the present study, we examined the role of each repair pathway in the formation of chromosome aberration by using knockout DT40 cell lines.
We constructed Ku70-/- and Rad54-/- cell lines and chromosome aberration that induced in G1 or G2 phase by X-irradiation was examined.
The results in G2 phase irradiation showed that higher frequency of chromatid type aberration was observed in Rad54-/- cells than that in other cell lines. This suggests that HR in which Rad54 plays an important role is important for the relief of formation of chromatid type aberration. When cells were irradiated in G1 phase, higher yield of chromosome type aberration was observed in Ku70-/- cells. Interestingly, dicentric was suppressed in Ku70-/- cells in G1 irradiation. These results suggest that chromosome type aberration is suppressed by NHEJ in which Ku70 plays an important role, although Ku70 is important for formation of dicentric.
