ATAD5 functions as a regulatory platform for Ub-PCNA deubiquitination

Abstract

Ubiquitination status of proliferating cell nuclear antigen (PCNA) is crucial for regulating DNA lesion bypass. After the resolution of fork stalling, PCNA is subsequently deubiquitinated, but the underlying mechanism remains undefined. We found that the DNA- loaded Ub-PCNA through distinct DNA- binding and PCNA- binding motifs. facilitating the deubiquitination of DNA- loaded Ub-PCNA. ATAD5 also enhances the Ub-PCNA deubiquitination by USP7 and USP11 through specific interactions. had increased sensitivity to DNA- damaging agents. Our results ultimately reveal that from the DNA in order to safely deactivate the DNA repair process.