Bacteriophages (phages) have a tremendous capacity for shaping the ecology and evolution of bacterial communities. Temperate phages, in particular, have the potential to rewire the biology of their bacterial hosts during lysogenic replication when they take the form of an integrated or episomal prophage. In contrast, temperate phages can act as time-bombs upon induction of lytic replication, leading to the depletion of certain bacterial lineages. There are many unanswered questions about the factors that regulate temperate phage life cycles and as a result, how they balance their beneficial and antagonistic relationships with their hosts. In part, this is because many phage genomes and the functions they encode remain uncharacterized (creating so-called “viral dark matter”). To bridge this knowledge gap, I am probing for molecular modulators of phage life cycles using the P2 temperate phage as a model system. P2 is a DNA-damage inducible phage that encodes a small peptide (which we have named ‘PhiR’) that has homology to a bacterial regulator of RecA and the DNA damage SOS response. In this study, I assess how PhiR may function to buffer the bacterial SOS response through RecA interactions that ultimately time prophage induction. I have also found evidence that PhiR may be involved in regulating RecA-dependent adaptive mutagenesis. Lastly, I uncover how widely distributed PhiR-like homologs are across different bacterial lineages and their potential to enhance bacterial fitness. Ultimately, this work highlights how temperate phage tune into the bacterial SOS response to regulate their life cycles and influence bacterial ecology and evolution.