DNA damage in the germline is a double-edged sword. On one hand, induced double-strand breaks establish the foundation for meiotic recombination, which is essential for proper chromosome segregation. On the other hand, double-strand breaks can also pose a significant challenge for genome stability. Within the germline, transposable elements are powerful agents of double-strand break formation. How different types of DNA damage are resolved within the germline is poorly understood. For example, little is known about the relationship between the frequency of double-stranded breaks, both endogenous and exogenous, and the decision to repair DNA through one of many pathways, including crossing over and gene conversion. We aim to use the Drosophila virilis hybrid dysgenesis model to determine how recombination landscapes change under transposable element activation. In this system, a cross between two strains of D. virilis with divergent transposable element loads results in the hybrid dysgenesis phenotype, which includes the germline activation of diverse transposable elements, reduced fertility and male recombination. However, only one direction of the cross results in hybrid dysgenesis. This allows us to examine recombination in genetically identical F1 females; those with baseline levels of programmed DNA damage and those with an increased level of DNA damage resulting from transposable element proliferation. We are using multiplexed shotgun genotyping to map crossover events to compare the recombination landscapes of hybrid dysgenic and non-hybrid dysgenic individuals. Finally, we are examining whether the additional crossovers are mitotic or meiotic in origin by characterizing the degree to which increased levels of recombination arising from transposable element activation are clustered among siblings.