During mitosis, chromosomes undergo extensive structural changes resulting in the formation of compact cylindrical bodies and in the termination of the bulk of DNA-dependent metabolic activities. Therefore, DNA lesions that interfere with processes such as DNA replication and transcription in interphase are not expected to pose a major threat to genome stability in mitosis. There are, however, a few exceptions. DNA replication and repair intermediates that physically interconnect the sister chromatids jeopardize faithful chromosome segregation and need to be resolved before the onset of anaphase. In addition, dicentric chromosomes can form chromatin bridges and induce breakage-fusion-breakage cycles with dire consequences for genome stability. Finally, chromosome breaks that escape the G2/M DNA damage checkpoint or emerge early in mitosis may result in lagging acentric DNA fragments that mis-segregate and form micronuclei when cells exit from mitosis. Both chromatin bridges and micronuclei are potential sources of a mutational cascade that results in massive chromosomal instability and significantly contributes to genomic complexity. Here, we review recent progress in our understanding of the origins and consequences of chromosome bridges and micronuclei and the mechanisms by which cells suppress them.

在有丝分裂过程中，染色体经历广泛的结构变化，导致形成紧凑的圆柱体并终止大量依赖 DNA 的代谢活动。因此，干扰诸如间期 DNA 复制和转录等过程的 DNA 损伤预计不会对有丝分裂中的基因组稳定性构成重大威胁。然而，也有一些例外。DNA 复制和修复中间体在物理上相互连接姐妹染色单体会危及忠实的染色体分离，需要在后期开始之前解决。此外，双着丝粒染色体可以形成染色质桥并诱导断裂-融合-断裂循环，对基因组稳定性造成可怕后果。最后，逃离 G2/M DNA 损伤检查点或在有丝分裂早期出现的染色体断裂可能导致滞后的无着丝粒 DNA 片段，当细胞退出有丝分裂时，这些片段会错误分离并形成微核。染色质桥和微核都是突变级联的潜在来源，会导致大量染色体不稳定并显着增加基因组的复杂性。在这里，我们回顾了我们在理解染色体桥和微核的起源和后果以及细胞抑制它们的机制方面的最新进展。