ArticleProceedings of the National Academy of Sciences of the United States of America2016
Unreplicated DNA remaining from unperturbed S phases passes through mitosis for resolution in daughter cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 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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Who cites it
84 citing papers in PubMed, 136 citations in OpenAlex.
- Article
- Defects in the DNA Damage Response of Patient-derived Endometriosis Stromal Cells.bioRxiv : the preprint server for biology · 2025Article
- Endogenous p21 levels protect genomic stability by suppressing both excess and restrained nascent DNA syntheses.Science advances · 2025Article
- CDK-driven phosphorylation of TRAIP is essential for mitotic replisome disassembly and MiDAS.Nucleic acids research · 2025Article
- Loss of G1-phase CDK-inhibition biases instability between genomic regions by unevenly reducing activity among replication origins.iScience · 2025Article
- Article
- Article
- Mitotic chromatin marking governs the segregation of DNA damage.Nature communications · 2025Article
- 53BP1-the 'Pandora's box' of genome integrity.DNA repair · 2024Review
- Replication stress induces POLQ-mediated structural variant formation throughout common fragile sites after entry into mitosis.Nature communications · 2024Article
- Inferring replication timing and proliferation dynamics from single-cell DNA sequencing data.Nature communications · 2024Article
- Mitotic chromatin marking governs asymmetric segregation of DNA damage.bioRxiv : the preprint server for biology · 2024Article
- BRCA1 and 53BP1 regulate reprogramming efficiency by mediating DNA repair pathway choice at replication-associated double-strand breaks.Cell reports · 2024Article
- Tryptophanyl-tRNA synthetase-1 (WARS-1) depletion and high tryptophan concentration lead to genomic instability in Caenorhabditis elegans.Cell death discovery · 2024Article
- Review
- Article
- Replication stress in mammalian embryo development, differentiation, and reprogramming.Trends in cell biology · 2023Review
- Review
- Article
- Methylated histones on mitotic chromosomes promote topoisomerase IIα function for high fidelity chromosome segregation.iScience · 2023Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 3 countries.
Funding
Abstract
To prevent rereplication of genomic segments, the eukaryotic cell cycle is divided into two nonoverlapping phases. During late mitosis and G1 replication origins are "licensed" by loading MCM2-7 double hexamers and during S phase licensed replication origins activate to initiate bidirectional replication forks. Replication forks can stall irreversibly, and if two converging forks stall with no intervening licensed origin-a "double fork stall" (DFS)-replication cannot be completed by conventional means. We previously showed how the distribution of replication origins in yeasts promotes complete genome replication even in the presence of irreversible fork stalling. This analysis predicts that DFSs are rare in yeasts but highly likely in large mammalian genomes. Here we show that complementary strand synthesis in early mitosis, ultrafine anaphase bridges, and G1-specific p53-binding protein 1 (53BP1) nuclear bodies provide a mechanism for resolving unreplicated DNA at DFSs in human cells. When origin number was experimentally altered, the number of these structures closely agreed with theoretical predictions of DFSs. The 53BP1 is preferentially bound to larger replicons, where the probability of DFSs is higher. Loss of 53BP1 caused hypersensitivity to licensing inhibition when replication origins were removed. These results provide a striking convergence of experimental and theoretical evidence that unreplicated DNA can pass through mitosis for resolution in the following cell cycle.
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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.