The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index.
53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress
Open accessAbstract
Completion of genome duplication is challenged by structural and topological barriers that impede progression of replication forks. Although this can seriously undermine genome integrity, the fate of DNA with unresolved replication intermediates is not known. Here, we show that mild replication stress increases the frequency of chromosomal lesions that are transmitted to daughter cells. Throughout G1, these lesions are sequestered in nuclear compartments marked by p53-binding protein 1 (53BP1) and other chromatin-associated genome caretakers. We show that the number of such 53BP1 nuclear bodies increases after genetic ablation of BLM, a DNA helicase associated with dissolution of entangled DNA. Conversely, 53BP1 nuclear bodies are partially suppressed by knocking down SMC2, a condensin subunit required for mechanical stability of mitotic chromosomes. Finally, we provide evidence that 53BP1 nuclear bodies shield chromosomal fragile sites sequestered in these compartments against erosion. Together, these data indicate that restoration of DNA or chromatin integrity at loci prone to replication problems requires mitotic transmission to the next cell generations.
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Cites
The DNA-damage response in human biology and disease
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Self-citationDNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation
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Self-citationActivation of the DNA damage checkpoint and genomic instability in human precancerous lesions
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Self-citationAn Oncogene-Induced DNA Damage Model for Cancer Development
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Self-citationOncogene-induced senescence is a DNA damage response triggered by DNA hyper-replication
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53BP1 Inhibits Homologous Recombination in Brca1-Deficient Cells by Blocking Resection of DNA Breaks
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Cited by
ATR prohibits replication catastrophe by preventing global exhaustion of RPA
Toledo, L. I., Altmeyer, M., Rask, M.-B., Lukas, C., Larsen, D. H., Povlsen, L. K., Bekker-Jensen, S., Mailand, N., Bartek, J., & Lukas, J. (2013) · Cell · doi:10.1016/j.cell.2013.10.043 · Cited by 911
Self-citationReplication stress is a potent driver of functional decline in ageing haematopoietic stem cells
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Self-citationLiquid demixing of intrinsically disordered proteins is seeded by poly(ADP-ribose)
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Self-citationMechanisms of Oncogene-Induced Replication Stress: Jigsaw Falling into Place
Kotsantis, P., Petermann, E., & Boulton, S. J. (2018) · Cancer Discovery · doi:10.1158/2159-8290.cd-17-1461 · Cited by 416
Metadata
- Authors
- Lukas, C., Savic, V., Bekker-Jensen, S., Doil, C., Neumann, B., Sølvhøj Pedersen, R., Grøfte, M., Chan, K. L., Hickson, I. D., Bartek, J., & Lukas, J.
- Venue
- Nature Cell Biology
- Published
- 2011-02-13
- Volume
- 13
- Issue
- 3
- Pages
- 243-253
- ISSN
- 1465-7392 (ISSN-L)
- 1476-4679
- OpenAlex
- W2025555587
- Cited by
- 667
- References
- 52
- FWCI
- 18.93
- Type
- journal article
- Language
- en
- Open access
- green
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- Lukas, C., Savic, V., Bekker-Jensen, S., Doil, C., Neumann, B., Sølvhøj Pedersen, R., Grøfte, M., Chan, K. L., Hickson, I. D., Bartek, J., & Lukas, J. (2011). 53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress. Nature Cell Biology. https://doi.org/10.1038/ncb2201
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