ArticleNucleic acids research2022
3D chromatin connectivity underlies replication origin efficiency in mouse embryonic stem cells.
Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Replication origin flexibility: a tool to mitigate the hazards of excess replication.Trends in genetics : TIG · 2026Review
- Microhomology-mediated end joining acts directly on replication forks to repair single-ended double-strand breaks.Molecular cell · 2026Article
- Multiple strategies to resolve the conflict between replication and transcription in mammalian cells.Nucleic acids research · 2026Article
- Analysis of Chromatin Structure Using Network Approaches: A Step-by-Step Guide.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Master transcription-factor binding sites constitute the core of early replication control elements.The EMBO journal · 2025Article
- Global chromatin reorganization and regulation of genes with specific evolutionary ages during differentiation and cancer.Nucleic acids research · 2025Article
- Histone variant macroH2A1 regulates synchronous firing of replication origins in the inactive X chromosome.Nucleic acids research · 2024Article
- Global chromatin reorganization and regulation of genes with specific evolutionary ages during differentiation and cancer.bioRxiv : the preprint server for biology · 2024Article
- PHF2 regulates genome topology and DNA replication in neural stem cells via cohesin.Nucleic acids research · 2024Article
- DNA replication and replication stress response in the context of nuclear architecture.Chromosoma · 2024Review
Corrections and comments
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Authors and funding
14 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mammalian cells, chromosomal replication starts at thousands of origins at which replisomes are assembled. Replicative stress triggers additional initiation events from 'dormant' origins whose genomic distribution and regulation are not well understood. In this study, we have analyzed origin activity in mouse embryonic stem cells in the absence or presence of mild replicative stress induced by aphidicolin, a DNA polymerase inhibitor, or by deregulation of origin licensing factor CDC6. In both cases, we observe that the majority of stress-responsive origins are also active in a small fraction of the cell population in a normal S phase, and stress increases their frequency of activation. In a search for the molecular determinants of origin efficiency, we compared the genetic and epigenetic features of origins displaying different levels of activation, and integrated their genomic positions in three-dimensional chromatin interaction networks derived from high-depth Hi-C and promoter-capture Hi-C data. We report that origin efficiency is directly proportional to the proximity to transcriptional start sites and to the number of contacts established between origin-containing chromatin fragments, supporting the organization of origins in higher-level DNA replication factories.
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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.