Research Paper Volume 12, Issue 24 pp 24872—24893
Age-associated deficient recruitment of 53BP1 in G1 cells directs DNA double-strand break repair to BRCA1/CtIP-mediated DNA-end resection
Figure 5. Model for the age-related shift in the DSB repair pathway choice in G1 cells. In response to DSB induction, 53BP1 is recruited to the break site in G1 cells from YDs and promotes repair by canonical non-homologous end-joining (c-NHEJ). Instead, in G1 AD cells, the deficient recruitment of 53BP1 permits the ectopic recruitment of BRCA1 to some DSBs, followed by CtIP-mediated DNA-end resection and RPA coating of the ssDNA. However, RAD51 loading is inhibited in these G1 cells and homologous recombination (HR) cannot be launched. Thus, DSBs from ADs that have suffered DNA-end resection in G1 become substrates for alternative DSB repair mechanisms, such as the alternative end-joining (Alt-EJ).