Burcu Inanc, Qingming Fang, Joel F Andrews, Xuemei Zeng, Jennifer Clark, Jianfeng Li, Nupur B Dey, Md Ibrahim, Peter Sykora, Zhongxun Yu, Andrea Braganza, Marcel Verheij, Jos Jonkers, Nathan A Yates, Conchita Vens, Robert W Sobol
The multitude of DNA lesion types, and the nuclear dynamic context in which they occur, present a challenge for genome integrity maintenance as this requires the engagement of different DNA repair pathways. Specific 'repair controllers' that facilitate DNA repair pathway crosstalk between double strand break (DSB) repair and base excision repair (BER), and regulate BER protein trafficking at lesion sites, have yet to be identified. We find that DNA polymerase β (Polβ), crucial for BER, is ubiquitylated in a BER complex-dependent manner by TRIP12, an E3 ligase that partners with UBR5 and restrains DSB repair signaling...
April 10, 2024: bioRxiv