ArticleNucleic acids research2014
A concomitant loss of dormant origins and FANCC exacerbates genome instability by impairing DNA replication fork progression.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Molecular regulation of DNA damage and repair in female infertility: a systematic review.Reproductive biology and endocrinology : RB&E · 2024Pooled it
- FANCD2 restrains fork progression and prevents fragility at early origins upon re-replication.Nature communications · 2026Article
- Potential role of Fanconi anemia pathway in the pathogenesis of endometrial cancer (Review).Molecular medicine reports · 2025Review
- 53BP1-the 'Pandora's box' of genome integrity.DNA repair · 2024Review
- Mitotic DNA Synthesis in Untransformed Human Cells Preserves Common Fragile Site Stability via a FANCD2-Driven Mechanism That Requires HELQ.Journal of molecular biology · 2023Article
- UBE2T resolves transcription-replication conflicts and protects common fragile sites in primordial germ cells.Cellular and molecular life sciences : CMLS · 2023Article
- Fanconi anemia proteins participate in a break-induced-replication-like pathway to counter replication stress.Nature structural & molecular biology · 2021Article
- Under-Replicated DNA: The Byproduct of Large Genomes?Cancers · 2020Review
- SMC5/6 acts jointly with Fanconi anemia factors to support DNA repair and genome stability.EMBO reports · 2020Article
- Mitotic DNA Synthesis Is Differentially Regulated between Cancer and Noncancerous Cells.Molecular cancer research : MCR · 2019Article
- Around and beyond 53BP1 Nuclear Bodies.International journal of molecular sciences · 2017Review
- Dormant origins as a built-in safeguard in eukaryotic DNA replication against genome instability and disease development.DNA repair · 2017Review
- Break induced replication in eukaryotes: mechanisms, functions, and consequences.Critical reviews in biochemistry and molecular biology · 2017Review
- Human somatic cells deficient for RAD52 are impaired for viral integration and compromised for most aspects of homology-directed repair.DNA repair · 2017Article
- Rescue from replication stress during mitosis.Cell cycle (Georgetown, Tex.) · 2017Review
- Simvastatin and Atorvastatin inhibit DNA replication licensing factor MCM7 and effectively suppress RB-deficient tumors growth.Cell death & disease · 2017Article
- Human RIF1 and protein phosphatase 1 stimulate DNA replication origin licensing but suppress origin activation.EMBO reports · 2017Article
- Order from clutter: selective interactions at mammalian replication origins.Nature reviews. Genetics · 2017Review
- Endogenous DNA Damage Leads to p53-Independent Deficits in Replicative Fitness in Fetal Murine Fancd2Stem cell reports · 2016Article
- The Fanconi anaemia pathway: new players and new functions.Nature reviews. Molecular cell biology · 2016Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Accumulating evidence suggests that dormant DNA replication origins play an important role in the recovery of stalled forks. However, their functional interactions with other fork recovery mechanisms have not been tested. We previously reported intrinsic activation of the Fanconi anemia (FA) pathway in a tumor-prone mouse model (Mcm4chaos3) with a 60% loss of dormant origins. To understand this further, we introduced a null allele of Fancc (Fancc-), encoding a member of the FA core complex, into the Mcm4chaos3 background. Primary embryonic fibroblasts double homozygous for Mcm4chaos3 and Fancc- (Mcm4chaos3/chaos3;Fancc-/-) showed significantly increased levels of markers of stalled/collapsed forks compared to either single homozygote. Interestingly, a loss of dormant origins also increased the number of sites in which replication was delayed until prophase, regardless of FA pathway activation. These replication defects coincided with substantially elevated levels of genome instability in Mcm4chaos3/chaos3;Fancc-/- cells, resulting in a high rate of perinatal lethality of Mcm4chaos3/chaos3;Fancc-/- mice and the accelerated tumorigenesis of surviving mice. Together, these findings uncover a specialized role of dormant origins in replication completion while also identifying important functional overlaps between dormant origins and the FA pathway in maintaining fork progression, genome stability, normal development and tumor suppression.
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Registered trials
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