Abstract:
:Recruitment of RAD18 to stalled replication forks facilitates monoubiquitination of PCNA during S-phase, promoting translesion synthesis at sites of UV irradiation-induced DNA damage. In this study, we show that RAD18 is also recruited to ionizing radiation (IR)-induced sites of DNA double-strand breaks (DSBs) forming foci which are co-localized with 53BP1, NBS1, phosphorylated ATM, BRCA1 and gamma-H2AX. RAD18 associates with 53BP1 and is recruited to DSB sites in a 53BP1-dependent manner specifically during G1-phase, RAD18 monoubiquitinates KBD domain of 53BP1 at lysine 1268 in vitro. A monoubiquitination-resistant 53BP1 mutant harboring a substitution at lysine 1268 is not retained efficiently at the chromatin in the vicinity of DSBs. In Rad18-null cells, retention of 53BP1 foci, efficiency of DSB repair and post-irradiation viability are impaired compared with wild-type cells. Taken together, these results suggest that RAD18 promotes 53BP1-directed DSB repair by enhancing retention of 53BP1, possibly through an interaction between RAD18 and 53BP1 and the modification of 53BP1.
journal_name
Nucleic Acids Resjournal_title
Nucleic acids researchauthors
Watanabe K,Iwabuchi K,Sun J,Tsuji Y,Tani T,Tokunaga K,Date T,Hashimoto M,Yamaizumi M,Tateishi Sdoi
10.1093/nar/gkp082subject
Has Abstractpub_date
2009-04-01 00:00:00pages
2176-93issue
7eissn
0305-1048issn
1362-4962pii
gkp082journal_volume
37pub_type
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