TI - RAD18 promotes DNA double strand break repair during G1 phase through chromatin retention of 53BP1 . AB - 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 .