Document Type

Open Access Thesis

Embargo Period


Degree Program


Degree Type

Master of Science (M.S.)

Year Degree Awarded


Month Degree Awarded



Double strand breaks (DSB) are a common source of DNA damage in both prokaryotes and eukaryotes. If they are not repaired or are repaired incorrectly, they can lead to cell death (bacteria) or cancer (humans). In Escherichia coli, repair of DSB are typically accomplished via homologous recombination and mediated by RecA. This repair pathway, among others, is associated with activation of the SOS response. DNA adenine methyltransferase (dam) mutants have an increased number of DSB and, therefore, are notorious for being RecA-dependent for viability. Here, we show that the synthetic lethality of Δdam/ΔrecA is suppressed when clpP is removed, suggesting that there is a protein, normally degraded by ClpXP, which is preventing DSB from occurring.

First Advisor

Steven Sandler

Second Advisor

M. Sloan Siegrist

Third Advisor

Yasu Morita