The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Dynamic assembly and sustained retention of 53BP1 at the sites of DNA damage are controlled by Mdc1/NFBD1
Open accessAbstract
53BP1 is a key component of the genome surveillance network activated by DNA double strand breaks (DSBs). Despite its known accumulation at the DSB sites, the spatiotemporal aspects of 53BP1 interaction with DSBs and the role of other DSB regulators in this process remain unclear. Here, we used real-time microscopy to study the DSB-induced redistribution of 53BP1 in living cells. We show that within minutes after DNA damage, 53BP1 becomes progressively, yet transiently, immobilized around the DSB-flanking chromatin. Quantitative imaging of single cells revealed that the assembly of 53BP1 at DSBs significantly lagged behind Mdc1/NFBD1, another DSB-interacting checkpoint mediator. Furthermore, short interfering RNA-mediated ablation of Mdc1/NFBD1 drastically impaired 53BP1 redistribution to DSBs and triggered premature dissociation of 53BP1 from these regions. Collectively, these in vivo measurements identify Mdc1/NFBD1 as a key upstream determinant of 53BP1's interaction with DSBs from its dynamic assembly at the DSB sites through sustained retention within the DSB-flanking chromatin up to the recovery from the checkpoint.
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Cites
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Methylated lysine 79 of histone H3 targets 53BP1 to DNA double-strand breaks
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“Next, we exploited the recent discovery that the Tudor domain of 53BP1 directly interacts with H3-dmK79 ( Huyen et al., 2004 ), thereby determining the productive accumulation of 53BP1 in the IR-induced foci.”
BackgroundResultInfluentialThe MRE11 complex: at the crossroads of DNA repair and checkpoint signalling
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MDC1 is a mediator of the mammalian DNA damage checkpoint
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The BRCT Domain Is a Phospho-Protein Binding Domain
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MDC1 is required for the intra-S-phase DNA damage checkpoint
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Self-citation
Cited by
Nuclear envelope rupture and repair during cancer cell migration
Denais, C. M., Gilbert, R. M., Isermann, P., McGregor, A. L., te Lindert, M., Weigelin, B., Davidson, P. M., Friedl, P., Wolf, K., & Lammerding, J. (2016) · Science · doi:10.1126/science.aad7297 · Cited by 1,318
-H2AX in recognition and signaling of DNA double-strand breaks in the context of chromatin
Kinner, A., Wu, W., Staudt, C., & Iliakis, G. (2008) · Nucleic Acids Research · doi:10.1093/nar/gkn550 · Cited by 1,256
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d'Adda di Fagagna, F. (2008) · Nature Reviews Cancer · doi:10.1038/nrc2440 · Cited by 1,170
Orchestration of the DNA-Damage Response by the RNF8 Ubiquitin Ligase
Kolas, N. K., Chapman, J. R., Nakada, S., Ylanko, J., Chahwan, R., Sweeney, F. D., Panier, S., Mendez, M., Wildenhain, J., Thomson, T. M., et al. (2007) · Science · doi:10.1126/science.1150034 · Cited by 894
DNA damage checkpoints: from initiation to recovery or adaptation
Bartek, J., & Lukas, J. (2007) · Current Opinion in Cell Biology · doi:10.1016/j.ceb.2007.02.009 · Cited by 784
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Metadata
- Authors
- Bekker-Jensen, S., Lukas, C., Melander, F., Bartek, J., & Lukas, J.
- Venue
- The Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2005-07-11
- Volume
- 170
- Issue
- 2
- Pages
- 201-211
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- OpenAlex
- W2049262839
- Cited by
- 275
- References
- 12
- FWCI
- 9.22
- Type
- journal article
- Language
- en
- Open access
- green
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- Bekker-Jensen, S., Lukas, C., Melander, F., Bartek, J., & Lukas, J. (2005). Dynamic assembly and sustained retention of 53BP1 at the sites of DNA damage are controlled by Mdc1/NFBD1. The Journal of Cell Biology. https://doi.org/10.1083/jcb.200503043
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