ArticleNature communications2025
DNA replication timing reveals genome-wide features of transcription and fragility.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Telomere-driven replicative crisis is driven by large-scale changes in genomic architecture.Genome research · 2026Article
- RepliSage: a stochastic graph-based framework for 3D chromatin modeling across the cell cycle.Nucleic acids research · 2026Article
- Decoding DNA metabolism and its clinical relevance through the lens of high-throughput sequencing assays.Medical review (2021) · 2026Review
- Computational Insights into SIRT1: Elucidating Mutational Impact on SIRT1-RECQL4 Structural Dynamics.Cell biochemistry and biophysics · 2026Article
- The landscape of structural variation in pediatric cancer.Cancer cell · 2026Article
- REPLAY: A reproducible and user-friendly application for DNA replication timing analysis from Repli-seq data.bioRxiv : the preprint server for biology · 2026Article
- Structural Modeling of Protein-DNA Interactions Underlying Genome Copy Number Variation in Nanoviruses.Computational and structural biotechnology journal · 2026Article
- DNA replication timing reveals genome-wide features of transcription and fragility.Nature communications · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
DNA replication in humans requires precise regulation to ensure accurate genome duplication and maintain genome integrity. A key indicator of this regulation is replication timing, which reflects the interplay between origin firing and fork dynamics. We present a high-resolution (1-kilobase) mathematical model that infers firing rate distributions from Repli-seq timing data across multiple cell lines, enabling a genome-wide comparison between predicted and observed replication. Notably, regions where the model and data diverge often overlap fragile sites and long genes, highlighting the influence of genomic architecture on replication dynamics. Conversely, regions of strong concordance are associated with open chromatin and active promoters, where elevated firing rates facilitate timely fork progression and reduce replication stress. In this work, we provide a valuable framework for exploring the structural interplay between replication timing, transcription, and chromatin organisation, offering insights into the mechanisms underlying replication stress and its implications for genome stability and disease.
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Registered trials
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