Increased UV‐induced SCEs but normal repair of DNA damage in p53‐deficient mouse cells

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Abstract
UV‐induced sister chromatid exchanges (SCEs) in p53‐deficient mouse cells were studied to obtain more evidence regarding the involvement of p53 protein in the DNA repair pathway as a checkpoint protein. After 5 J/m2 UV irradiation, mutant‐type homozygous cells for p53‐deficiency showed the same number of SCEs as the heterozygous and wild‐type homozygous cells. In the heterozygous and wild‐type homozygous cells, no further increase of SCEs was observed after 10 J/m2 UV irradiation. In contrast, in mutant‐type homozygous cells about twice as many SCEs were induced by 10 J/m2 UV as by 5 J/m2 UV. In mutant‐type homozygous cells, fractions of S‐phase cells decreased just after 10 J/m2 UV irradiation, but recovered to higher than control levels within a short time, while in heterozygous and wild‐type homozygous cells, the decrease in S‐phase cells was prolonged by more than 6 hr and no increase above control levels was observed. Although no difference in UV sensitivity and repair of UV‐induced DNA damage was found among the 3 genotypes, which were determined by the relative colony‐forming ability after UV irradiation and removal of thymine dimers and (6‐4) photoproducts from cellular DNA, our data strongly suggest an impaired checkpoint function in p53‐deficient cells when DNA is damaged.