DNA is constantly exposed to damage-causing agents. The SOS DNA damage response in Escherichia coli is regulated by the LexA protein, which controls the expression of more than 50 different genes. One of the many genes regulated by the SOS response encodes the protein of unknown function YbfE. Previous work in our lab has shown ybfE is essential to cell survival after exposure to the alkylating agents styrene oxide and chloroacetaldehyde. YbfE has been shown to cause a striking decrease in cell survival upon overexpression. To identify genetic interactions, a series of knockout strains have been investigated to determine whether deletion of any one gene alleviates the lethality associated with overexpression of ybfE. To date, assays in strains harboring deletions of mutS, uvrC, and uvrA proteins have not suppressed the lethal overexpression phenotype. However, advancements have been made in overcoming this lethality as work continues to obtain purified protein for further characterization. In addition, sensitivity studies with hydroxyurea, which inhibits DNA replication without inducing DNA damage, have been conducted. HU interacts with ribonucleotide reductase preventing the conversion of ribonucleotides to deoxyribonucleotides, leading to a depletion of available dNTPs. This depletion halts replication and initiates a series of cellular responses resulting in an increase in the production of reactive oxygen species. Deletion of the ybfE gene confers resistance to HU, suggesting a role for YbfE in DNA metabolism. Further investigation into protein interactions and the role of YbfE in the SOS response are ongoing. These studies will provide further insights into the role ybfE plays in the SOS response to DNA damage.

Characterization of LexA-regulated protein YbfE in E. coli

256th National Meeting (2018)

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