A P53-DEPENDENT MOUSE SPINDLE CHECKPOINT
A P53-DEPENDENT MOUSE SPINDLE CHECKPOINT
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DOI：
10.1126/science.7871434
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发表时间：
1995-03-03
期刊：
影响因子：
56.9
通讯作者：
REID, BJ
中科院分区：
文献类型：
--
作者：
CROSS, SM;SANCHEZ, CA;REID, BJ
细胞周期检查点通过在之前的事件尚未完成时在细胞周期的特定阶段引起停滞来提高遗传保真度。肿瘤抑制基因P53被认为与G(1)检查点有关。为了研究P53是否也参与有丝分裂检查点，来自P53缺陷的小鼠胚胎的培养成纤维细胞被暴露于纺锤体抑制剂。成纤维细胞在没有完成染色体分离的情况下，经过多轮DNA合成，形成四倍体酸性八倍体细胞。P53基因缺失也与体内四倍体的发生有关。这些结果表明，小鼠P53是纺锤体检查点的组成部分，确保了二倍体的维持。
Cell cycle checkpoints enhance genetic fidelity by causing arrest at specific stages of the cell cycle when previous events have not been completed. The tumor suppressor p53 has been implicated in a G(1) checkpoint. To investigate whether p53 also participates in a mitotic checkpoint, cultured fibroblasts from p53-deficient mouse embryos were exposed to spindle inhibitors. The fibroblasts underwent multiple rounds of DNA synthesis without completing chromosome segregation, thus forming tetraploid acid octaploid cells. Deficiency of p53 was also associated with the development of tetraploidy in vivo. These results suggest that murine p53 is a component of a spindle checkpoint that ensures the maintenance of diploidy.