DNA replication timing reveals genome-wide features of transcription and fragility

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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Publication Details

Journal
Nature Communications
Published
2025-05-19
DOI
https://doi.org/10.1038/s41467-025-59991-w
Citations
4
Primary Topic
DNA Repair Mechanisms
Type
article
Field-Weighted Citation Impact
3.22

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article

DNA replication timing reveals genome-wide features of transcription and fragility

Francisco Berkemeier, Peter R. Cook, Michael A. Boemo
4 citations
Nature Communications
DNA Repair Mechanisms
3.22
article

DNA replication timing reveals genome-wide features of transcription and fragility

Francisco Berkemeier, Peter R. Cook, Michael A. Boemo
article en
4 citations

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.

Nature CommunicationsVol. 16(1)
University of Cambridge (GB), University of Oxford (GB)
Queen Mary University of London, Dell EMC, Leverhulme Trust, Engineering and Physical Sciences Research Council
Openalex Percentile: Top 8%
DNA Repair Mechanisms
3.22
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