ABSTRACT
Germline DNA damage is a double-edged sword. Programmed double-strand breaks establish the foundation for meiotic recombination and chromosome segregation. However, double-strand breaks also pose a significant challenge for genome stability. Because of this, meiotic double-strand break formation is tightly regulated. However, natural selection can favor selfish behavior in the germline and transposable elements can cause double-strand breaks independent of the carefully regulated meiotic process. To understand how the regulatory mechanisms of meiotic recombination accommodate unregulated transposition, we have characterized the female recombination landscape in a syndrome of hybrid dysgenesis in Drosophila virilis. In this system, a cross between two strains of D. virilis with divergent transposable element and piRNA profiles results in germline transposition of diverse transposable elements, reduced fertility, and male recombination. We sought to determine how increased transposition during hybrid dysgenesis might perturb the meiotic recombination landscape. Our results show that the overall frequency and distribution of meiotic recombination is extremely robust to germline transposable element activation. However, we also find that hybrid dysgenesis can result in mitotic recombination within the female germline. Overall, these results show that landscape of meiotic recombination may be insensitive to the DNA damage caused by transposition during early development.
Footnotes
A new statistical analysis of mitotic recombination was added, as well as description of causative excision events. This was enabled with a new PacBio assembly of Strain 160.