ArticleCell cycle (Georgetown, Tex.)2014
Establishment of a replication fork barrier following induction of DNA binding in mammalian cells.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 53 citations in OpenAlex.
- R-PLA enables enhanced detection of R-loops in mammalian cells using proximity ligation.Cell reports methods · 2026Article
- Illuminating the genome: emerging approaches in CRISPR-Cas live-cell imaging.Nucleic acids research · 2026Review
- Visualizing DNA repair factor recruitment at sites of transcription in single cells.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2026Article
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- Ubiquitination of the histone variant mH2A1.2 prevents toxic RAD18 accumulation at a subset of genomic loci upon replication stress.Molecular cell · 2025Article
- TRIM24 directs replicative stress responses to maintain ALT telomeres via chromatin signaling.Molecular cell · 2025Article
- Live genome imaging by CRISPR engineering: progress and problems.Experimental & molecular medicine · 2025Review
- Transgenerational Tracking of Chromosomes from Micronuclei.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Elucidation of the molecular mechanism of the breakage-fusion-bridge (BFB) cycle using a CRISPR-dCas9 cellular model.Nucleic acids research · 2024Article
- Article
- Control of DNA replication in vitro using a reversible replication barrier.Nature protocols · 2024Article
- Aberrant DNA repair reveals a vulnerability in histone H3.3-mutant brain tumors.Nucleic acids research · 2024Article
- FIRRM cooperates with FIGNL1 to promote RAD51 disassembly during DNA repair.Science advances · 2023Article
- Characterization of Unidirectional Replication Forks in the Mouse Genome.International journal of molecular sciences · 2023Article
- A kinesin-based approach for inducing chromosome-specific mis-segregation in human cells.The EMBO journal · 2023Article
- Review
- Interaction with TopBP1 Is Required for Human Papillomavirus 16 E2 Plasmid Segregation/Retention Function during Mitosis.Journal of virology · 2022Article
- Chemically Induced Chromosomal Interaction (CICI) method to study chromosome dynamics and its biological roles.Nature communications · 2022Article
- DNA damage responses that enhance resilience to replication stress.Cellular and molecular life sciences : CMLS · 2021Review
- RNF168 E3 ligase participates in ubiquitin signaling and recruitment of SLX4 during DNA crosslink repair.Cell reports · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Understanding the mechanisms that lead to replication fork blocks (RFB) and the means to bypass them is important given the threat that they represent for genome stability if inappropriately handled. Here, to study this issue in mammals, we use integrated arrays of the LacO and/or TetO as a tractable system to follow in time a process in an individual cell and at a single locus. Importantly, we show that induction of the binding by LacI and TetR proteins, and not the presence of the repeats, is key to form the RFB. We find that the binding of the proteins to the arrays during replication causes a prolonged persistence of replication foci at the site. This, in turn, induces a local DNA damage repair (DDR) response, with the recruitment of proteins involved in double-strand break (DSB) repair such as TOPBP1 and 53BP1, and the phosphorylation of H2AX. Furthermore, the appearance of micronuclei and DNA bridges after mitosis is consistent with an incomplete replication. We discuss how the many DNA binding proteins encountered during replication can be dealt with and the consequences of incomplete replication. Future studies exploiting this type of system should help analyze how an RFB, along with bypass mechanisms, are controlled in order to maintain genome integrity.
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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.