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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Premature condensation induces breaks at the interface of early and late replicating chromosome bands bearing common fragile sites.
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Premature condensation induces breaks at the interface of early and late replicating chromosome bands bearing common fragile sites.

机译：过早的凝结在带有常见脆弱位点的早期和晚期复制染色体带的界面处引起断裂。

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摘要

Various studies suggest a tight relationship between chromosome rearrangements driving tumor progression and breaks at loci called common fragile sites. Most of these sites are induced after perturbation of the replication dynamics, notably by aphidicolin treatment. We have mapped the majority of these sites to the interface of R and G bands, which calls into question the previous assignment of aphidicolin-sensitive sites to R bands. This observation suggests that most of them correspond to loci that ensure the transition between early and late replicating domains. We show that calyculin A, which triggers chromosome condensation at any phase of the cell cycle but does not markedly impair replication, induces damage in the chromosomes of human lymphocytes treated in G(2) but not in G(1) phase. We demonstrate that these lesions colocalize with those induced by aphidicolin treatment. Hence, common fragile site stability is compromised, whether aphidicolin delays replication or calyculin A advances condensation. We also show that, in cells that go through an unperturbed S phase, completion of their replication and/or replication-associated chromatin reorganization occur all along the G(2) phase, which may explain their inability to condense properly after calyculin A treatment during this phase of the cell cycle.
机译：各种研究表明，驱动肿瘤进展的染色体重排与称为常见脆弱位点的基因座断裂之间存在紧密的联系。这些位置中的大多数是在复制动力学受到干扰后被诱导的，特别是通过蚜虫二甲酚处理。我们已经将这些位点的大部分映射到R和G谱带的界面，这使以前对Aphidicolin敏感的位点分配到R谱带产生了疑问。该观察结果表明，它们大多数对应于确保早期和晚期复制域之间过渡的基因座。我们表明，calyculin A，在细胞周期的任何阶段触发染色体浓缩，但不会明显损害复制，诱导了在G（2）阶段而非G（1）阶段处理的人类淋巴细胞的染色体损伤。我们证明这些损伤与由蚜虫碱治疗引起的损伤共定位。因此，无论是蚜虫碱延迟复制还是calyculin A促进缩合，普通的脆弱位点稳定性都会受到损害。我们还显示，在经历不受干扰的S期的细胞中，它们的复制和/或与复制相关的染色质重组的完成过程一直发生在G（2）阶段，这可能解释了它们在进行Calyculin A处理后无法正确凝结细胞周期的这一阶段。

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