Figure 7: Graphic summary and a mitochondrial BER model.
From: A domain in human EXOG converts apoptotic endonuclease to DNA-repair exonuclease
(a) Structural basis for hEXOG activity. (b) A proposed model for mitochondrial DNA long-patch (LP) BER and its difference from the nuclear LP-BER. In mitochondria, EXOG exerts 5'-exonuclease activity at the abasic site and generates a 2-3 nt gap on dsDNA, which is an optimal substrate for Polγ to perform gap-filling synthesis. In contrast, nuclear LP-BER depends on the strand displacement activity of the DNA polymerase and FEN1 cleaves the DNA flap.
