We established fibroblast cultures from p53-deficient mouse embryos, which were originally constructed by Dr. S. Aizawa (Kumamoto Univ.). These p53-deficient fibroblasts showed the same sensitivity to UV and X-ray as wild-type fibroblasts. There was no difference between repair activity of UV-induced DNA damages in p53-deficient and wild-type cells, either. However, UV-induced sister chromatid exchanges were significantly increased and delay of entering S-phase after UV-irradiation was reduced in p53-deficient cells indicating abnormality in the checkpoint function of the cell cycle in p53-deficient cells. We also used the supF gene on a shuttle vector to analyze UV-induced mutations in p53-deficient cells. Although frequencies of UV-induced mutations were not different between p53-deficient and wild-type cells, distributions of base-substitution mutations on the supF gene were different.