Why do cells sometimes choose to repair DNA damage using strategies that result in changes to the genetic sequence? This is the central question that drives our lab’s research. We use Drosophila melanogaster as a model organism to investigate how different DNA repair and DNA damage tolerance proteins are utilized to both maintain genome stability and generate genetic diversity. Specifically, we are interested in how various DNA lesions, such as base modifications, double-strand breaks, and interstrand crosslinks, are recognized and repaired in various tissues and developmental stages of the animal. A current focus of the lab is the characterization of an error-prone, alternative end-joining pathway that utilizes a multifunctional protein named DNA polymerase theta to fix double-strand breaks. We are also applying tissue- and developmental stage-specific methods to induce DNA damage and to study how cellular context affects replication and repair of the damaged DNA.