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DSB (Im)mobility and DNA Repair Compartmentalization in Mammalian Cells

机译：哺乳动物细胞中的DSB（Im）迁移率和DNA修复区室化

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Chromosomal translocations are considered as causal in approximately 20% of cancers. Therefore, understanding their mechanisms of formation is crucial in the prevention of carcinogenesis. The first step of translocation formation is the concomitant occurrence of double-strand DNA breaks (DSBs) in two different chromosomes. DSBs can be repaired by different repair mechanisms, including error-free homologous recombination (HR), potentially error-prone non-homologous end joining (NHEJ) and the highly mutagenic alternative end joining (alt-EJ) pathways. Regulation of DNA repair pathway choice is crucial to avoid genomic instability. In yeast, DSBs are mobile and can scan the entire nucleus to be repaired in specialized DNA repair centers or if they are persistent, in order to associate with the nuclear pores or the nuclear envelope where they can be repaired by specialized repair pathways. DSB mobility is limited in mammals; therefore, raising the question of whether the position at which a DSB occurs influences its repair. Here, we review the recent literature addressing this question. We first present the reports describing the extent of DSB mobility in mammalian cells. In a second part, we discuss the consequences of non-random gene positioning on chromosomal translocations formation. In the third part, we discuss the mobility of heterochromatic DSBs in light of our recent data on DSB repair at the nuclear lamina, and finally, we show that DSB repair compartmentalization at the nuclear periphery is conserved from yeast to mammals, further pointing to a role for gene positioning in the outcome of DSB repair. When regarded as a whole, the different studies reviewed here demonstrate the importance of nuclear architecture on DSB repair and reveal gene positioning as an important parameter in the study of tumorigenesis. (c) 2014 Elsevier Ltd.All rights reserved.
机译：在大约20％的癌症中，染色体易位被认为是原因。因此，了解其形成机制对于预防癌变至关重要。易位形成的第一步是在两个不同的染色体中同时发生双链DNA断裂（DSB）。 DSB可以通过不同的修复机制进行修复，包括无错误的同源重组（HR），容易出错的非同源末端连接（NHEJ）和高度诱变的替代末端连接（alt-EJ）途径。 DNA修复途径选择的调节对于避免基因组不稳定至关重要。在酵母中，DSB是可移动的，可以扫描要在专门的DNA修复中心修复的整个核，或者如果它们是持久性的，则可以与核孔或核被膜结合，以便可以通过专门的修复途径对其进行修复。 DSB的流动性在哺乳动物中受到限制;因此，提出了一个问题，即DSB发生的位置是否会影响其维修。在这里，我们回顾了有关该问题的最新文献。我们首先提出描述哺乳动物细胞中DSB迁移程度的报告。在第二部分中，我们讨论了非随机基因定位对染色体易位形成的影响。在第三部分中，我们根据最近有关核层的DSB修复的数据讨论了异色DSB的迁移性，最后，我们证明了在核外围对DSB的修复分区是保守的，从酵母到哺乳动物都是保守的，进一步指出了基因定位在DSB修复结果中的作用。从整体上看，本文综述的不同研究表明核结构对DSB修复的重要性，并揭示了基因定位是肿瘤发生研究中的重要参数。 （c）2014 Elsevier Ltd.保留所有权利。

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