作者: Susanna Stroik , Eric A Hendrickson
DOI: 10.1016/J.GDE.2020.02.010
关键词:
摘要: Telomere fusions inevitably arise as a cell’s last-ditch effort to protect exposed chromosomal ends when telomeres are lost due aging-associated erosion, breakage, failed replication, or plethora of other cellular mistakes. Fusion an end another telomere presumably presents superficially attractive option the cell opposed alternative impending degradation unprotected terminus. However, allowed progress mitosis these fusion events subsequently foster non-disjunction bridge:breakage — both which drive highly pathogenic genomic instability and additional translocations. Thus, question becomes how and, most importantly, is there mechanism available resolve bridges such that proper repair, not instability, results? Recent evidence suggests formation, then resolution of, ultrafine may facilitate this process.