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High-resolution mapping of mitotic DNA synthesis regions and common fragile sites in the human genome through direct sequencing

查看全文 作　　者：Morgane [1]Macheret;Rahul [2]Bhowmick;Katarzyna [1]Sobkowiak;Laura [1]Padayachy;Jonathan [1]Mailler;Ian [2]D.Hickson;Thanos [1]D.Halazonetis 高影响力作者 机构地区：[1]Department of Molecular Biology,University of Geneva,1205,Geneva,Switzerland;[2]Center for Chromosome Stability and Center for Healthy Aging,Department of Cellular and Molecular Medicine,University of Copenhagen,Blegdamsvej 3B,2200,Copenhagen N,Denmark高影响力机构 出　　处：《Cell Research》索引2020年第30卷第11期,共12页高影响力期刊 基　　金：This study was supported by grants from the Swiss National Science Foundation(160734)to T.D.H.and from the Danish National Research Foundation(DNRF115);the Nordea Foundation,and the Novo Nordisk Foundation to I.D.H. 摘　　要：DNA replication stress,a feature of human cancers,often leads to instability at specific genomic loci,such as the common fragile sites(CFSs).Cells experiencing DNA replication stress may also exhibit mitotic DNA synthesis(MiDAS).To understand the physiological function of MiDAS and its relationship to CFSs,we mapped,at high resolution,the genomic sites of MiDAS in cells treated with the DNA polymerase inhibitor aphidicolin.Sites of MiDAS were evident as well-defined peaks that were largely conserved between cell lines and encompassed all known CFSs.The MiDAS peaks mapped within large,transcribed,origin-poor genomic regions.In cells that had been treated with aphidicolin,these regions remained unreplicated even in late S phase;MiDAS then served to complete their replication after the cells entered mitosis.Interestingly,leading and lagging strand synthesis were uncoupled in MiDAS,consistent with MiDAS being a form of break-induced replication,a repair mechanism for collapsed DNA replication forks.Our results provide a better understanding of the mechanisms leading to genomic instability at CFSs and in cancer cells. 关 键 词：SYNTHESIS SITES REPAIR
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