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Chromothripsis: Breakage-fusion-bridge over and over again

机译：毛细血管痉挛：断续融合桥一遍又一遍

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摘要

The acquisition of massive but localized chromosome translocations, a phenomenon termed chromothripsis, has received widespread attention since its discovery over a year ago. Until recently, chromothripsis was believed to originate from a single catastrophic event, but the molecular mechanisms leading to this event are yet to be uncovered. Because a thorough interpretation of the data are missing, the phenomenon itself has wrongly acquired the status of a mechanism used to justify many kinds of complex rearrangements. Although the assumption that all translocations in chromothripsis originate from a single event has met with criticism, satisfactory explanations for the intense but localized nature of this phenomenon are still missing. Here, we show why the data used to describe massive catastrophic rearrangements are incompatible with a model comprising a single event only and propose a molecular mechanism in which a combination of known cellular pathways accounts for chromothripsis. Instead of a single traumatic event, the protection of undamaged chromosomes by telomeres can limit repetitive breakage-fusion-bridge events to a single chromosome arm. Ultimately, common properties of chromosomal instability, such as aneuploidy and centromere fission, might establish the complex genetic pattern observed in this genomic state.
机译：自从一年多前被发现以来，大规模但局部的染色体易位的获得被人们广泛关注。直到最近，人们仍认为色杆菌病起源于单个灾难性事件，但导致该事件的分子机制尚未被发现。由于缺少对数据的透彻解释，因此现象本身已错误地获得了用来证明多种复杂重排合理性的机制的地位。尽管所有关于染色体脱色病的易位性起源于单个事件的假设都遭到了批评，但是对于这种现象的强烈但局部的性质，仍然缺乏令人满意的解释。在这里，我们展示了为什么用于描述大规模灾难性重排的数据与仅包含单个事件的模型不兼容，并提出了一种分子机制，其中已知细胞途径的结合导致了色杆菌病。端粒对未损坏染色体的保护不是单个创伤事件，而是可以将重复的断裂-融合-桥事件限制在单个染色体臂上。最终，染色体不稳定性的共同特性，例如非整倍性和着丝粒分裂，可能会建立在这种基因组状态下观察到的复杂遗传模式。

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