A New Mode of Mitotic Surveillance.
A New Mode of Mitotic Surveillance.
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DOI：
10.1016/j.tcb.2017.01.004
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发表时间：
2017-05
影响因子：
19
通讯作者：
Holland AJ
中科院分区：
文献类型：
--
作者：
Lambrus BG;Holland AJ
细胞已经进化出一定的预防措施，以在有丝分裂期间保存它们的基因组内容，并避免潜在的致癌错误。除了已建立的DNA损伤和纺锤体组装检查点外，最近的观察还发现了另一个有丝分裂失败安全机制，称为有丝分裂监视途径。这一途径触发细胞周期停滞，阻止潜在不适合的子代细胞的生长，并被延长的有丝分裂和中心体丢失激活。最近的全基因组筛查令人惊讶地发现，53BP1和USP28作用于p53的上游，通过有丝分裂监视途径介导信号传递。在这里，我们回顾了我们对这一故障安全机制的理解进展，并讨论了53BP1和USP28如何在这一途径中发挥非典型作用。
Cells have evolved certain precautions to preserve their genomic content during mitosis and avoid potentially oncogenic errors. Aside from the well-established DNA damage and spindle assembly checkpoints, recent observations have identified an additional mitotic fail safe, referred to as the mitotic surveillance pathway. This pathway triggers a cell cycle arrest to block the growth of potentially unfit daughter cells, and is activated by both prolonged mitosis and centrosome loss. Recent genome-wide screens surprisingly revealed that 53BP1 and USP28 act upstream of p53 to mediate signaling through the mitotic surveillance pathway. Here, we review advances in our understanding of this fail-safe, and discuss how 53BP1 and USP28 adopt non-canonical roles to function in this pathway.