Telomere fusions inevitably arise as a cell's last-ditch effort to protect exposed chromosomal ends when telomeres are lost due to aging-associated erosion, breakage, failed replication, or a plethora of other cellular mistakes. Fusion of an exposed chromosomal end to another telomere presumably presents a superficially attractive option to the cell as opposed to the alternative of the impending degradation of the unprotected chromosomal terminus. However, when allowed to progress to mitosis these fusion events subsequently foster non-disjunction or bridge:breakage events - both of which drive highly pathogenic genomic instability and additional chromosomal translocations. Thus, the question becomes how and when telomere fusion events arise and, most importantly, is there a mechanism available to resolve these telomere bridges such that proper repair, and not genomic instability, results? Recent evidence suggests that the formation, and then the resolution of, ultrafine bridges may facilitate this process.

中文翻译：

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端粒融合和易位：桥梁太远？

当端粒由于衰老相关的侵蚀、断裂、复制失败或过多的其他细胞错误而丢失时，端粒融合不可避免地成为细胞保护暴露的染色体末端的最后努力。暴露的染色体末端与另一个端粒的融合可能为细胞提供了表面上有吸引力的选择，而不是未受保护的染色体末端即将降解的替代方案。然而，当允许进行有丝分裂时，这些融合事件随后会促进不分离或桥：断裂事件——这两者都会导致高致病性基因组不稳定性和额外的染色体易位。因此，问题变成了端粒融合事件如何以及何时发生，最重要的是，是否有一种机制可以解决这些端粒桥，从而导致适当的修复，而不是基因组不稳定？最近的证据表明，超细桥的形成和分解可能会促进这一过程。