Polβ/XRCC1 heterodimerization dictates DNA damage recognition and basal Polβ protein levels without interfering with mouse viability or fertility.

ABSTRACT: DNA Polymerase β (Polβ) performs two critical enzymatic steps during base excision repair (BER) - gap filling (nucleotidyl transferase activity) and gap tailoring (dRP lyase activity). X-ray repair cross complementing 1 (XRCC1) facilitates the recruitment of Polβ to sites of DNA damage through an evolutionarily conserved Polβ/XRCC1 interaction interface, the V303 loop. While previous work describes the importance of the Polβ/XRCC1 interaction for human Polβ protein stability and recruitment to sites of DNA damage, the impact of disrupting the Polβ/XRCC1 interface on animal viability, physiology, and fertility is unknown. Here, we characterized the effect of disrupting Polβ/XRCC1 heterodimerization in mice and mouse cells by complimentary approaches. First, we demonstrate, via laser micro-i

SUBMITTER: Koczor CA 

PROVIDER: S-EPMC9992099 | biostudies-literature | 2023 Mar

REPOSITORIES: biostudies-literature