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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >P53 DEFICIENCY DOES NOT AFFECT THE ACCUMULATION OF POINT MUTATIONS IN A TRANSGENE TARGET
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P53 DEFICIENCY DOES NOT AFFECT THE ACCUMULATION OF POINT MUTATIONS IN A TRANSGENE TARGET

机译：P53缺陷不会影响转基因目标中点突变的累积

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摘要

DNA repair is required by organisms to prevent the accumulation of mutations and to maintain the integrity of genetic information. Mammalian cells that have been treated with agents that damage DNA have an increase in p53 levels, a p53-dependent arrest at G(1) in the cell cycle, and a p53-dependent apoptotic response. It has been hypothesized that this block in cell cycle progression is necessary to allow time for DNA repair or to direct the damaged cell to an apoptotic pathway. This hypothesis predicts that p53-deficient cells would have an abnormal apoptotic response and exhibit a ''mutator'' phenotype. Using a sensitive assay for the accumulation of point mutations, small deletions, and insertions, we have directly tested whether p53-deficient cells exhibit an increased frequency of mutation before and after exposure to DNA-damaging agents. We report that wild-type and p53-deficient fibroblasts, thymocytes, and tumor tissue have indistinguishable rates of point mutation accumulation in a transgenic lacI target gene. These results suggest that the role of p53 in G(1) checkpoint control and tumor suppression does not affect the accumulation of point mutations. [References: 36]
机译：生物体需要进行DNA修复，以防止突变的积累并保持遗传信息的完整性。已经用破坏DNA的试剂处理过的哺乳动物细胞的p53水平升高，在细胞周期中G（1）处p53依赖的停滞以及p53依赖的凋亡反应。假设细胞周期进程中的这种阻滞是必要的，以便有时间进行DNA修复或将受损细胞引导至凋亡途径。该假设预测p53缺陷的细胞将具有异常的凋亡反应并表现出“突变”表型。使用针对点突变，小缺失和插入积累的灵敏测定法，我们直接测试了p53缺陷细胞在暴露于DNA损伤剂之前和之后是否表现出增加的突变频率。我们报告说，野生型和p53缺陷的成纤维细胞，胸腺细胞和肿瘤组织在转基因lacI目标基因中具有不可区分的点突变积累率。这些结果表明，p53在G（1）检查站控制和肿瘤抑制中的作用不影响点突变的积累。 [参考：36]

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