21Germline DNA damage is a double-edged sword. Programmed double-strand breaks establish 22 the foundation for meiotic recombination and chromosome segregation. However, double-strand 23 breaks also pose a significant challenge for genome stability. Because of this, meiotic double-24 strand break formation is tightly regulated. However, natural selection can favor selfish behavior 25 in the germline and transposable elements can cause double-strand breaks independent of the 26 carefully regulated meiotic process. To understand how the regulatory mechanisms of meiotic 27 recombination accommodate unregulated transposition, we have characterized the female 28 recombination landscape in a syndrome of hybrid dysgenesis in Drosophila virilis. In this 29 system, a cross between two strains of D. virilis with divergent transposable element and piRNA 30 profiles results in germline transposition of diverse transposable elements, reduced fertility, and 31 male recombination. We sought to determine how increased transposition during hybrid 32 dysgenesis might perturb the meiotic recombination landscape. Our results show that the overall 33 frequency and distribution of meiotic recombination is extremely robust to germline transposable 34 element activation. However, we also find that hybrid dysgenesis can result in mitotic 35 recombination within the female germline. Overall, these results show that landscape of meiotic 36 recombination may be insensitive to the DNA damage caused by transposition during early 37 development. 38 2011). Moreover, TEs can activate the DNA damage response within developing germline stem 51 cells and alter stem cell fate (Chen et al. 2007;Wylie et al. 2014; Tasnim and Kelleher 2018). 52 53The harmful effects of TEs are especially evident in syndromes of hybrid dysgenesis, where 54 sterility can arise in intraspecific crosses between males carrying TEs and females that lack them 55 (Bingham et al. 1982; Bucheton et al. 1984;Yannopoulos et al. 1987; Lozovskaya et al. 1990). 56 Hybrid dysgenesis is the result of TE activation in the absence of maternal repression by interacting RNAs (piRNAs) (Aravin et al. 2007; Brennecke et al. 2008). The piRNA system of 58 genome defense requires maternal deposition of piRNA to successfully silence TEs across 59 generations. The combination of unrecognized TEs introduced to a naive genome via sperm and 60 the absence of corresponding piRNAs in the egg results in TE activation and hybrid dysgenesis 61 5 (Brennecke et al. 2008). A unique syndrome of hybrid dysgenesis in D. virilis is observed in 62 intraspecific crosses between males of an inducing strain (designated strain 160) and reactive 63 strain females (designated strain 9) (Lozovskaya et al. 1990). The primary TE family responsible 64 for inducing dysgenesis remains unknown and sterility appears to be due to the mass activation 65 of several TE families abundant in strain 160 but not strain 9. At least four elements are proposed 66 to contribute significantly to dysgenesis: Penelope, Helena, Paris, an...