fig2

Figure 2. The role of WRN RECQL helicase in switching DSB repair pathway choice. WRN plays a crucial role in promoting c-NHEJ and suppressing alt-NHEJ. In HRR, WRN plays an indispensable role in late DSB resection and CHK1-mediated RAD51 loading in HRR. In the absence of WRN, regulation is switched to p38-MAPK-mediated RAD51 loading during HRR in cancer cells. The dashed arrow shows the compensatory pathway activated in the absence of WRN. DSB: Double strand break; SSB: single strand break; NHEJ: nonhomologous end joining; cNHEJ: canonical NHEJ; alt-NHEJ: alternative NHEJ; HRR: homologous recombination repair; CHK: checkpoint kinase 1; RAD5: DNA repair protein RAD51 homolog 1; MRE: meiotic recombination 11; CTIP: CtBP (carboxy-terminal binding protein) interacting protein; ATM: ataxia telangiectasia mutated; ATR: ataxia telangiectasia and Rad3 related.