Cells have evolved certain precautions to preserve their genomic content during mitosis and avoid potentially oncogenic errors. Besides the well-established DNA damage checkpoint and spindle assembly checkpoint (SAC), recent observations have identified an additional mitotic failsafe 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 failsafe and discuss how 53BP1 and USP28 adopt noncanonical roles to function in this pathway.

细胞已经进化出一定的预防措施，以在有丝分裂期间保持其基因组含量并避免潜在的致癌错误。除了完善的DNA损伤检查点和纺锤体装配检查点（SAC）外，最近的观察还发现了另一种有丝分裂故障保险，称为有丝分裂监视途径。该途径触发细胞周期停滞，以阻止可能不合适的子代细胞的生长，并通过延长的有丝分裂和中心体损失而被激活。最近的全基因组筛选令人惊讶地发现53BP1和USP28在p53的上游起作用，通过有丝分裂监视途径介导信号传导。在这里，我们回顾了我们对这种故障保险的理解的进展，并讨论了53BP1和USP28如何采用非规范性角色在该途径中发挥作用。