Isolation of a DNA Ligase Mutant from L1210 Cells

Abstract

Current evidence suggests that the ADP-ribosylation of chromatin proteins is involved in DNA repair [2]. Much of this evidence comes from the use of inhibitors of ADPRT, such as 3-aminobenzamide (3AB), which retards DNA strand rejoining following DNA damage and potentiates the cytotoxicity of DNA damaging agents. Alkylation damage increases DNA ligase activity, predominantly that of DNA ligase II. This increase is prevented by ADPRT inhibitors. We have previously suggested that the requirement for ADPRT in DNA repair is at the ligation step [1].