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Dynamic assembly and sustained retention of 53BP1 at the sites of DNA damage are controlled by Mdc1/NFBD1
S Bekker-Jensen, C Lukas, F Melander, J Bartek, J Lukas
Language English Country United States
NLK
Free Medical Journals
from 1962 to 6 months ago
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from 1962 to 6 months ago
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from 1962 to 6 months ago
Open Access Digital Library
from 1955-01-25
Open Access Digital Library
from 1959-01-01
Open Access Digital Library
from 1962-01-01
Medline Complete (EBSCOhost)
from 2005-03-28 to 2011-09-19
PubMed
16009723
Knihovny.cz E-resources
- MeSH
- Chromatin physiology MeSH
- DNA-Binding Proteins physiology genetics MeSH
- Phosphoproteins physiology genetics MeSH
- Intracellular Signaling Peptides and Proteins physiology genetics MeSH
- Nuclear Proteins physiology genetics MeSH
- Microscopy, Confocal MeSH
- Humans MeSH
- RNA, Small Interfering physiology MeSH
- Mice MeSH
- Cell Line, Tumor MeSH
- DNA Damage * MeSH
- Recombinant Fusion Proteins genetics metabolism MeSH
- Trans-Activators physiology genetics MeSH
- Protein Transport MeSH
- Protein Binding MeSH
- Green Fluorescent Proteins genetics MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Mice MeSH
- Animals MeSH
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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- $a 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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