Journal
JOURNAL OF CELL SCIENCE
Volume 126, Issue 6, Pages 1297-1306Publisher
COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/jcs.096701
Keywords
Cell cycle; Checkpoint; DNA damage; DNA replication; Origin; Stress; Replication fork
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Funding
- Cancer Research UK
- European Research Council [249883-EUKDNAREP]
- Association for International Cancer Research [10-0270]
- EMBO long-term fellowship
- Cancer Research UK [15669] Funding Source: researchfish
- Worldwide Cancer Research [10-0270] Funding Source: researchfish
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DNA replication in eukaryotic cells initiates from multiple replication origins that are distributed throughout the genome. Coordinating the usage of these origins is crucial to ensure complete and timely replication of the entire genome precisely once in each cell cycle. Replication origins fire according to a cell-type-specific temporal programme, which is established in the G1 phase of each cell cycle. In response to conditions causing the slowing or stalling of DNA replication forks, the programme of origin firing is altered in two contrasting ways, depending on chromosomal context. First, inactive or 'dormant' replication origins in the vicinity of the stalled replication fork become activated and, second, the S phase checkpoint induces a global shutdown of further origin firing throughout the genome. Here, we review our current understanding on the role of dormant origins and the S phase checkpoint in the rescue of stalled forks and the completion of DNA replication in the presence of replicative stress.
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