ArticleCurrent biology : CB2015
Replication fork progression during re-replication requires the DNA damage checkpoint and double-strand break repair.
Article in Current biology : CB, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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, 33 citations in OpenAlex.
- Physiological re-replication during human stem cell differentiation.Cell death discovery · 2026Article
- FANCD2 restrains fork progression and prevents fragility at early origins upon re-replication.Nature communications · 2026Article
- The Drosophila histone variant H2Av facilitates Notch signaling activity in a two-tier regulatory fashion.Cell communication and signaling : CCS · 2025Article
- A non-tethering role for the Drosophila Pol θ linker domain in promoting damage resolution.Nucleic acids research · 2025Article
- Review
- Unscheduled DNA replication in G1 causes genome instability and damage signatures indicative of replication collisions.Nature communications · 2022Article
- Sirtuin5 protects colorectal cancer from DNA damage by keeping nucleotide availability.Nature communications · 2022Article
- Article
- Article
- Control of Eukaryotic DNA Replication Initiation-Mechanisms to Ensure Smooth Transitions.Genes · 2019Review
- MUS81 Participates in the Progression of Serous Ovarian Cancer Associated With Dysfunctional DNA Repair System.Frontiers in oncology · 2019Article
- Article
- Deoxyribonucleic Acid Damage and Repair: Capitalizing on Our Understanding of the Mechanisms of Maintaining Genomic Integrity for Therapeutic Purposes.International journal of molecular sciences · 2018Review
- Nuclear DNA Replication in Trypanosomatids: There Are No Easy Methods for Solving Difficult Problems.Trends in parasitology · 2017Review
- Polyteny: still a giant player in chromosome research.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2017Review
- DNA Replication Control DuringGenetics · 2017Review
- Looping-out mechanism for resolution of replicative stress at telomeres.EMBO reports · 2017Article
- Initiation of Drosophila chorion gene amplification requires Claspin and mus101, whereas Claspin, but not mus101, plays a major role during elongation.Developmental dynamics : an official publication of the American Association of Anatomists · 2017Article
- Review
- Multiple mechanisms contribute to double-strand break repair at rereplication forks in Drosophila follicle cells.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Replication origins are under tight regulation to ensure activation occurs only once per cell cycle [1, 2]. Origin re-firing in a single S phase leads to the generation of DNA double-strand breaks (DSBs) and activation of the DNA damage checkpoint [2-7]. If the checkpoint is blocked, cells enter mitosis with partially re-replicated DNA that generates chromosome breaks and fusions [5]. These types of chromosomal aberrations are common in numerous human cancers, suggesting that re-replication events contribute to cancer progression. It was proposed that fork instability and DSBs formed during re-replication are the result of head-to-tail collisions and collapse of adjacent replication forks [3]. However, previously studied systems lack the resolution to determine whether the observed DSBs are generated at sites of fork collisions. Here, we utilize the Drosophila ovarian follicle cells, which exhibit re-replication under precise developmental control [8-10], to model the consequences of re-replication at actively elongating forks. Re-replication occurs from specific replication origins at six genomic loci, termed Drosophila amplicons in follicle cells (DAFCs) [10-12]. Precise developmental timing of DAFC origin firing permits identification of forks at defined points after origin initiation [13, 14]. Here, we show that DAFC re-replication causes fork instability and generates DSBs at sites of potential fork collisions. Immunofluorescence and ChIP-seq demonstrate the DSB marker γH2Av is enriched at elongating forks. Fork progression is reduced in the absence of DNA damage checkpoint components and nonhomologous end-joining (NHEJ), but not homologous recombination. NHEJ appears to continually repair forks during re-replication to maintain elongation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.