The ubiquitin landscape at DNA double-strand breaks

Human Rad52 Promotes XPG-Mediated R-loop Processing to Initiate Transcription-Associated Homologous Recombination Repair

“…We found that ATM kinase activity is extensively required for the initiation of HRR, including TA-HRR ( Figure 4F). To define the roles of ATM in TA-HRR, we first tested the RNF8-and RNF168-dependent ubiquitin signaling cascade activated by the ATM kinase upon DSB induction (Jackson and Durocher, 2013;Messick and Greenberg, 2009). We found that neither RNF8 nor RNF168 KD affects the RPA recruitment after IR, suggesting that ATM-mediated activation of the ubiquitin signaling cascade is not required for the initiation of HRR ( Figure S5D).…”

The histone variant macroH2A1.1 is recruited to DSBs through a mechanism involving PARP1

“…Consequently, DSB repair requires significant remodeling of the chromatin to facilitate access to sites of DNA damage and to promote processing and repair of the DNA [1,2]. This reorganization of the chromatin landscape involves both chromatin remodeling ATPases [1,3] as well as histone modification, including acetylation of histone H4 by the Tip60 acetyltransferase [3,4] and ubiquitination of the chromatin by the RNF8 and RNF168 ubiquitin ligases [5]. These modifications function together to create open chromatin structures at sites of damage and to provide binding sites to recruit the brca1 complex and other proteins involved in DSB repair [2].…”

Human KIAA1018/FAN1 localizes to stalled replication forks via its ubiquitin-binding domain

“…14 Ubiquitin is widely utilized as a signaling molecule in eukaryotic cells in the context of several different types of DNA damage. [15][16][17][18][19][20] The presence of a ubiquitinbinding domain suggests the potential involvement of the UBZ domain in localization and/or regulation of FAN1. Because FAN1 contains both a nuclease and a ubiquitin-binding domain, it may be involved in genome stability.…”