Abstract:
: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.
journal_name
Cell Resjournal_title
Cell researchauthors
Macheret M,Bhowmick R,Sobkowiak K,Padayachy L,Mailler J,Hickson ID,Halazonetis TDdoi
10.1038/s41422-020-0358-xsubject
Has Abstractpub_date
2020-11-01 00:00:00pages
997-1008issue
11eissn
1001-0602issn
1748-7838pii
10.1038/s41422-020-0358-xjournal_volume
30pub_type
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