Abstract 1650 Investigating the function of plausible DNA polymerase protein Pol A2

DNA damage can disrupt cellular DNA replication mechanisms leading to increased mutagenesis, a hallmark of cancer. Based on homology models, Pol A2, a DNA polymerase protein from the bacterium Rothia dentocariosa, appears to play a role in the DNA damage response by allowing replication of damaged DNA to continue by bypassing lesions in a process called translesion synthesis (TLS). We have purified PolA2 and variants containing mutations in likely active site and steric gate residues. To characterize Pol A2, thermal shift assays were performed using the wild type PolA2 and variants.