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. Author manuscript; available in PMC: 2022 Jan 4.
Published in final edited form as: DNA Repair (Amst). 2020 Sep;93:102908. doi: 10.1016/j.dnarep.2020.102908

Fig. 3. LigI protein partners.

Fig. 3.

A. Linear schematic of LigI polypeptide showing the N-terminal binding sites for PCNA, PolĪ² and UHRF1 as well phosphorylated serine residues and an acetylated lysine residue. B. Interaction of LigI with PCNA is critical for the recruitment of LIgI to replication foci and the efficient joining of Okazaki fragments. Methylation of LigI by G9a is required for an interaction with UHRF1/DNMT1 that enables DNMT1 to methylate the newly synthesized DNA at the replication fork (white circles unmethylated cytosine; red circles, methylated cytosine. C. Upper panel, interaction of LigI with PCNA is critical for the repair of non-bulky lesions by the long patch BER pathway and the S-phase specific subpathway of NER. Middle panel, interaction of LigI with the hRad9-hRad1-hHus1 clamp stimulates DNA joining during long patch BER and may also occur in NER. Lower panel, LigI interacts with PolĪ² within a BER complex, suggesting a role for LigI in short patch BER.