ArticleNature cell biology2019
53BP1 nuclear bodies enforce replication timing at under-replicated DNA to limit heritable DNA damage.
Article in Nature cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 113 citations in OpenAlex.
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- BMI1 represses G-quadruplex DNA formation to maintain genomic stability during replication.The Journal of biological chemistry · 2026Article
- Macrophages promote aberrant DNA repair in multiple myeloma via the CXCL5/8-CXCR2 axis.Haematologica · 2026Article
- Defects in the DNA Damage Response of Patient-derived Endometriosis Stromal Cells.bioRxiv : the preprint server for biology · 2025Article
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- Mitotic chromatin marking governs the segregation of DNA damage.Nature communications · 2025Article
- Cell cycle progression of under-replicated cells.Nucleic acids research · 2025Article
- Transgenerational Tracking of Chromosomes from Micronuclei.Methods in molecular biology (Clifton, N.J.) · 2025Review
- 53BP1-the 'Pandora's box' of genome integrity.DNA repair · 2024Review
- RAD52 and ERCC6L/PICH have a compensatory relationship for genome stability in mitosis.PLoS genetics · 2024Article
- PPM1D activity promotes cellular transformation by preventing senescence and cell death.Oncogene · 2024Article
- Mitotic chromatin marking governs asymmetric segregation of DNA damage.bioRxiv : the preprint server for biology · 2024Article
- HDAC4 influences the DNA damage response and counteracts senescence by assembling with HDAC1/HDAC2 to control H2BK120 acetylation and homology-directed repair.Nucleic acids research · 2024Article
- Progeria-based vascular model identifies networks associated with cardiovascular aging and disease.Aging cell · 2024Article
- The dimeric deubiquitinase USP28 integrates 53BP1 and MYC functions to limit DNA damage.Nucleic acids research · 2024Article
14 more citing papers are in PubMed but not listed here.
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6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Failure to complete DNA replication is a stochastic by-product of genome doubling in almost every cell cycle. During mitosis, under-replicated DNA (UR-DNA) is converted into DNA lesions, which are inherited by daughter cells and sequestered in 53BP1 nuclear bodies (53BP1-NBs). The fate of such cells remains unknown. Here, we show that the formation of 53BP1-NBs interrupts the chain of iterative damage intrinsically embedded in UR-DNA. Unlike clastogen-induced 53BP1 foci that are repaired throughout interphase, 53BP1-NBs restrain replication of the embedded genomic loci until late S phase, thus enabling the dedicated RAD52-mediated repair of UR-DNA lesions. The absence or malfunction of 53BP1-NBs causes premature replication of the affected loci, accompanied by genotoxic RAD51-mediated recombination. Thus, through adjusting replication timing and repair pathway choice at under-replicated loci, 53BP1-NBs enable the completion of genome duplication of inherited UR-DNA and prevent the conversion of stochastic under-replications into genome instability.
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