ArticleNature communications2022
The mechanism of replication stalling and recovery within repetitive DNA.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- ERCC6 at the Transcription-Replication Interface: Integration of Transcription-Coupled Repair with Replication Stress Responses.International journal of molecular sciences · 2026Review
- In vitro reconstitution of chromatin replication recapitulates symmetric histone recycling.Nature communications · 2026Article
- Decoding DNA metabolism and its clinical relevance through the lens of high-throughput sequencing assays.Medical review (2021) · 2026Review
- The role of the nuclear pore complex in the stability of disease-related short tandem DNA repeats.Nucleic acids research · 2026Article
- AVITI sequencing of a four-generation CEPH/Utah pedigree confirms low mutation rates at homopolymer loci despite their low sequence complexity.Genome biology · 2026Article
- Exploring Genome-Wide Mutation Dynamics and Bacterial Cellulose Impairment inComputational and structural biotechnology journal · 2026Article
- Genomic Instability and Clonal Hematopoiesis in the Deep-Space Environment: The Role of Sex-Chromosome Asymmetry and High-LET Radiation.Current stem cell reports · 2026Article
- Base excision repair within structure-forming repeat sequences and its impact on cancer and other diseases.NAR cancer · 2025Review
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- Overcoming natural replication barriers formed by DNA structures and the role of repositioning to the nuclear periphery.DNA repair · 2025Review
- AVITI sequencing of a four-generation CEPH/Utah pedigree confirms low mutation rates at homopolymer loci despite their low sequence complexity.bioRxiv : the preprint server for biology · 2025Article
- G-quadruplex stabilization induces DNA breaks in pericentromeric repetitive DNA sequences in B lymphocytes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The DNA replication checkpoint limits Okazaki fragment accumulation to protect and restart stalled forks.Molecular cell · 2025Article
- Tandemly Repeated G-Quadruplex Structures in the Pseudorabies Virus Genome: Implications for Epiberberine-Based Antiviral Therapy.International journal of molecular sciences · 2025Article
- Deep visual proteomics reveals DNA replication stress as a hallmark of signet ring cell carcinoma.NPJ precision oncology · 2025Article
- DNA synthesis across DNA hairpins by human PrimPol.DNA repair · 2024Article
- NeoDesign: a computational tool for optimal selection of polyvalent neoantigen combinations.Bioinformatics (Oxford, England) · 2024Article
- Repetitive Sequence Stability in Embryonic Stem Cells.International journal of molecular sciences · 2024Review
- Control of DNA replication in vitro using a reversible replication barrier.Nature protocols · 2024Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Accurate chromosomal DNA replication is essential to maintain genomic stability. Genetic evidence suggests that certain repetitive sequences impair replication, yet the underlying mechanism is poorly defined. Replication could be directly inhibited by the DNA template or indirectly, for example by DNA-bound proteins. Here, we reconstitute replication of mono-, di- and trinucleotide repeats in vitro using eukaryotic replisomes assembled from purified proteins. We find that structure-prone repeats are sufficient to impair replication. Whilst template unwinding is unaffected, leading strand synthesis is inhibited, leading to fork uncoupling. Synthesis through hairpin-forming repeats is rescued by replisome-intrinsic mechanisms, whereas synthesis of quadruplex-forming repeats requires an extrinsic accessory helicase. DNA-induced fork stalling is mechanistically similar to that induced by leading strand DNA lesions, highlighting structure-prone repeats as an important potential source of replication stress. Thus, we propose that our understanding of the cellular response to replication stress may also be applied to DNA-induced replication stalling.
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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.