Document Type


Publication Date

Spring 2021


In Acinetocbacter baumannii bacteria, an error-prone DNA damage repair response is induced by the self-cleavage of the UmuDAb protein. Previous experiments indicating that a ddrR mutant becomes growth sensitive after DNA damage suggested that ddrR is also involved in this process. To explore this relationship, eight mutant strains of A. baumannii were made with different combinations of mutations in either ddrR and/or the adjacent gene, A1S_3662. Our experiment compared the growth of wild type cells to strains containing various mutations: DC4 (no gene mutations, just an antibiotic resistance marker, Kanr), DC5 (stop codon mutation in ddrR), and DC6 (both the Kanr and the ddrR stop codon). The objective of this experiment was to compare viable colony forming units (CFUs) per mL between strains after treatment with DNA-damaging mitomycin C (MMC). This data allowed for the growth sensitivity between strains to be numerically compared. Serial dilutions were made from overnight cultures for each strain, and spots of each dilution were plated onto LB plates. The plates were incubated overnight, after which the colonies in each spot were counted and the CFU/mL was calculated for each strain, with and without MMC treatment. Our results from strains DC4, DC5, and DC6 suggests that the Kanr gene inserted into the DC4 strain hinders growth more than the ddrR stop codon present in DC5 and DC6. This was observed in both treated and untreated DC4 strains. Although the DC4 colonies were smaller, they were more numerous than the other strains. These experiments will help identify the extent to which these genes may participate in the growth response after DNA damage in this opportunistic pathogen.