Prokaryotes possess a remarkable ability to respond to environmental stressors using simple genetic circuits that detect signals of stress and mount an appropriate response. The SOS pathway is an example of such a genetic circuit mediating error-prone DNA repair in response to DNA damage. Native control over the SOS pathway is orchestrated by the repressor-protease, LexA. Following a DNA damaging event, the damage sensor RecA activates LexA to undergo a self-cleavage reaction that results in LexA dissociation from SOS promoters and subsequent pathway activation. However, the inability to decouple upstream events – DNA damage and RecA activation – from LexA cleavage by genetic means alone has limited our ability to wholly understand how the SOS pathway contributes to repair, mutagenesis, and bacterial survival. We sought to overcome this limitation by designing a synthetic circuit to orthogonally control SOS activation independent of native signals. Chapter 2 describes the design of the synthetic circuit, in which an exogenously cleavable LexA variant was engineered by embedding a recognition site for TEV protease into the LexA flexible linker region. TEV expression was placed under the control of the small-molecule anhydrotetracycline (ATc), decoupling LexA cleavage from DNA damage and RecA. We show that addition of ATc to strains harboring our synthetic circuit permits small-molecule inducible UV resistance and inducible mutagenesis. Further, exploiting our ability to activate SOS genes independently of upstream events, we show that SOS pathway activation alone is insufficient for mutagenesis, but instead demonstrate the importance of a DNA damage nidus. In Chapter 3, as our circuit newly permits temporal separation of damage and repair, we utilize our circuit to probe the kinetics of UV-mediated cell death and the timeframe in which repair must occur to prevent lethality. We find delaying SOS activation results in a rapid time-dependent loss of viability and global promoter silencing, and that the rate of irreversible lethality is energy-dependent but protein synthesis- and replication-independent, shedding light on the potential mechanisms of UV-mediated cell death. Finally, in Chapter 4, we outline future uses for our synthetic circuit to dissect the roles of the SOS pathway in repair, mutagenesis, and other phenotypes.