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RNF8 Ubiquitylates Histones at DNA Double-Strand Breaks and Promotes Assembly of Repair Proteins
TLDR
It is suggested that MDC1-mediated and RNF8-executed histone ubiquitylation protects genome integrity by licensing the DSB-flanking chromatin to concentrate repair factors near the DNA lesions. Expand
RNF168 Binds and Amplifies Ubiquitin Conjugates on Damaged Chromosomes to Allow Accumulation of Repair Proteins
TLDR
Evidence is provided that, while RNF8 is necessary to trigger the DSB-associated ubiquitylation, it is not sufficient to sustain conjugated ubiquitin in this compartment, which defines a new pathway involving sequential ubiquitylations on damaged chromosomes and uncovers a functional cooperation between E3 ligases in genome maintenance. Expand
Chromatin relaxation in response to DNA double-strand breaks is modulated by a novel ATM- and KAP-1 dependent pathway
TLDR
It is shown that DSB formation is followed by ATM-dependent chromatin relaxation, which suggests that chromatin Relaxation is a fundamental pathway in the DNA-damage response and identifies its primary mediators. Expand
ATR Prohibits Replication Catastrophe by Preventing Global Exhaustion of RPA
Luis Ignacio Toledo,1 Matthias Altmeyer,1 Maj-Britt Rask,1 Claudia Lukas,1 Dorthe Helena Larsen,1 Lou Klitgaard Povlsen,2 Simon Bekker-Jensen,2 Niels Mailand,2 Jiri Bartek,3,4 and Jiri Lukas1,*Expand
Spatial organization of the mammalian genome surveillance machinery in response to DNA strand breaks
TLDR
It is proposed that subclassification of DSB regulators according to their residence sites provides a useful framework for understanding their involvement in diverse processes of genome surveillance. Expand
53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress
TLDR
It is shown that mild replication stress increases the frequency of chromosomal lesions that are transmitted to daughter cells, and evidence is provided that 53BP1 nuclear bodies shield chromosomal fragile sites sequestered in these compartments against erosion. Expand
Phosphorylation of SDT repeats in the MDC1 N terminus triggers retention of NBS1 at the DNA damage–modified chromatin
TLDR
It is suggested that phosphorylation of the SDT repeats in the MDC1 N terminus functions to recruit NBS1 and, thereby, increases the local concentration of MRN at the sites of chromosomal breakage. Expand
Mdc1 couples DNA double‐strand break recognition by Nbs1 with its H2AX‐dependent chromatin retention
TLDR
Mdc1 functions as an H2AX‐dependent interaction platform enabling a switch from transient, Mdc1‐independent recruitment of Nbs1 to DSBs towards sustained, MDC1‐dependent interactions with the surrounding chromosomal microenvironment. Expand
Assembly and function of DNA double-strand break repair foci in mammalian cells.
TLDR
Recent discoveries on the mechanisms that govern the formation of IRIF are focused on, and the implications of such findings are discussed in light of the understanding of the physiological importance of these structures. Expand
Dynamic assembly and sustained retention of 53BP1 at the sites of DNA damage are controlled by Mdc1/NFBD1
TLDR
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 D SB-flanking chromatin up to the recovery from the checkpoint. Expand
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