Fig. 7
From: Mutational signatures reveal the role of RAD52 in p53-independent p21-driven genomic instability
Prolonged p21WAF1/Cip1 expression promotes Rad52-dependent break-induced replication (BIR) and single strand annealing (SSA) repair of DNA double strand breaks (DSBs). a Reduced synthesis-dependent strand annealing (SDSA) in 96-h induced Saos2- and Li-Fraumeni-p21WAF1/Cip1Tet-ON cells. Flow cytometry analysis (FACS) after p21WAF1/Cip1 induction in cells stably expressing a DR-GFP report vector and following I-SceI-induced DSBs shows decreased SDSA activity (*p < 0.05, t-test; error bars indicate standard deviation; n = 5 experiments), regardless of Rad52 silencing. Similar manipulations in Saos2- and Li-Fraumeni-p21PCNA Tet-ON cells showed no differences in SDSA in these cells. b Increased BIR activity in 96-h induced Saos2- and Li-Fraumeni-p21WAF1/Cip1 Tet-ON cells. FACS after p21WAF1/Cip1 induction in cells stably expressing a BIR-GFP report vector and following I-SceI-induced DSBs shows increased BIR activity (*p < 0.05, t-test; error bars indicate standard deviation; n = 5 experiments) that is suppressed upon Rad52 silencing. Similar experiment in Saos2- and Li-Fraumeni-p21PCNA Tet-ON cells showed no effect on BIR function in these cells. c Increased SSA activity in 96-h induced Saos2- and Li-Fraumeni-p21WAF1/Cip1 Tet-ON cells. FACS after p21WAF1/Cip1 induction in cells stably expressing an SA-GFP report vector and following I-SceI-induced DSBs shows increased SSA activity (*p < 0.05, t-test; error bars indicate standard deviation; n = 5 experiments) that is dependent on Rad52. A similar experiment in Saos2- and Li-Fraumeni-p21PCNA Tet-ON cells showed no effect on SSA function in these cells