Genetic instability of p53-deficient mouse cells.
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.
Ishizaki
K
K
Laboratory of Experimental Radiology, Aichi Cancer Center Research Institute, Nagoya, Japan.
Mimaki
S
S
Nishizawa
K
K
D000818:Animals; D002453:Cell Cycle / Q000528:radiation effects; D002470:Cell Survival / Q000502:physiology* / Q000528:radiation effects; D005347:Fibroblasts; D016153:Genes, Suppressor; D005822:Genetic Vectors; D051379:Mice; D012343:RNA, Transfer / Q000096:biosynthesis; D014162:Transfection; D016159:Tumor Suppressor Protein p53 / Q000172:deficiency* / Q000502:physiology; D014466:Ultraviolet Rays; D014965:X-Rays
D016159:Tumor Suppressor Protein p53; C096275:supF tRNA; D012343:RNA, Transfer