In order to discover the role of the repair process of DNA double strand breaks on the induction of genomic instability, we investigated radiation-induced delayed chromosome aberrations in SCID mouse cells that defected in nonhomologous end-joining. Wild-type mouse cells and SCID mouse cells were irradiated with an equivalent 10% survival dose of X-rays, and then delayed chromosome aberrations, such as dicentrics and fragments, were scored over 20 cell divisions, postirradiation. The chromosome analysis indicated that radiosensitive SCID mouse cells are more susceptible to the induction of delayed chromosome aberrations than wild-type mouse cells, suggesting that the defect in nonhomologous end-joining promotes genomic instability. To elucidate the mechanism for the formation of delayed dicentrics in mouse cells, we found that telomere sequences remained at a fused position of two chromosomes in a dicentric using the telomere-FISH technique. The result revealed that radiation increases the frequency of delayed dicentrics, of which telomere sequences are retained at the fusion point, suggesting that radiation induces telomere dysfunction and that this telomere instability is involved in the formation of delayed chromosome aberrations. The telomere-FISH analysis also demonstrated that the SCID mouse cells are more susceptible to the induction of telomeric instability, suggesting that the DNA-dependent protein kinase (DNA-PK) catalytic subunit is involved in the maintenance of telomeres.