DNA is consistently damaged within the cell from a variety of outside sources, including ionizing radiation, ultraviolet radiation, and exposure to chemical agents. The cell has a number of repair pathways that recognize this damage and either chemically reverse or repair it by replacing individual base pairs, or whole segments of affected DNA. Another cellular mechanism involves Y-Family polymerases, which are highly conserved across many life forms, and are specialized to replicate damaged DNA without first repairing the damage itself. The larger binding pocket characteristic of these polymerases leads to significant decrease in fidelity when compared to traditional replicative polymerases, and this loss of fidelity within humans can lead to cancer and reduced efficacy of chemotherapy. This research focuses on the protein DinB, the E. coli ortholog of human Polymerase Kappa, which has been implicated in mutagenic antibiotic resistance. Building on previous research, nine compounds selected as potential DinB inhibitors were investigated for their effect on the survival of E. coli AB1157 wild type and ΔdinB cells. All but one inhibitor were well tolerated by the cells with no difference noted between the wild type and DinB knockout strains. This information will be built upon to further identify a promising Y-Family polymerase inhibitor. Future experimentation will involve assays to compare rates of spontaneous antibiotic resistance of E. coli cells in the presence of inhibitors to those found in the absence of them.

Effect of DinB inhibitors on Esherichia coli cell survival

Macromolecular Chemistry: The Second Century

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ACS Spring 2020 National Meeting & Expo

The official archive and repository for all ACS Meetings & Expositions abstracts and select posters or presentations.