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首页> 外文期刊>EMBO Journal >Early replication fragile sites: Where replication-transcription collisions cause genetic instability
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Early replication fragile sites: Where replication-transcription collisions cause genetic instability

机译：早期复制脆弱的网站:replication-transcription碰撞导致遗传不稳定

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Although it is known that replication stress causes genetic instability, the underlying mechanisms are not yet fully understood. A new study by Barlow et al (2013) used an elegant genome-wide chromatin immunoprecipitation approach to reveal that DNA lesions induced by replication stress occur predominantly in early replicating and actively transcribed gene clusters. These 'early replication fragile sites' (ERFS) can be the source for rearrangements commonly found in cancer, and represent a new type of fragile site, distinct from common fragile sites (CFS). Genetic instability is a threat to the integrity of DNA and underlies the genomic rearrangements that need to occur early in preneoplastic lesions in order to cause the genetic changes required for development into neoplastic disease. It has been demonstrated that cellular oncogenes, such as mos, cdc6, cyclin E and ras, not only provide proliferation signals but also induce replication stress associated with the formation of DNA double-strand breaks (DSBs).
机译：尽管众所周知,复制的压力引起遗传不稳定,底层机制尚未完全清楚。巴洛et al(2013)的研究使用了一个优雅全基因组染色质免疫沉淀反应方法泄露引起的DNA损伤复制应力主要发生在早期复制并积极转录基因集群。(小块土地)可重组的来源常见的癌症中,代表一个新的脆弱的网站类型,不同于常见的脆弱的网站(CFS)。DNA的完整性和构成威胁基因组重组需要提前发生在肿瘤出现前的病变引起发展所需的基因变化肿瘤疾病。细胞癌基因,如金属氧化物半导体,cdc 6,细胞周期素E和ras,不仅提供增殖信号但也导致复制相关的压力DNA双链断裂的形成(DSBs)。

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