This guest post is by Justin Blumenstiel on his preprint (with co-authors) When genomes collide: multiple modes of germline misregulation in a dysgenic syndrome of Drosophila virilis, available from bioRxiv here.

Does the activation of one transposable element (TE) family typically lead to the activation of many? If so, this would indicate a synergism between different TE families with significance for TE dynamics in natural populations. A standard model of TE dynamics typically takes into account population size, transposition rate (which may vary based on host defense) and selection against TE insertions. If the mobilization of one TE can lead to the mobilization of others, the transposition rate of one TE family could influence the transposition rate of others.

Hybrid dysgenic syndromes in Drosophila are an important model for TE dynamics when one TE family becomes mobilized. In the 1980’s, it was generally concluded that P element dysgenesis did not lead to mobilization of other TEs. However, studies in the D. virilis system of hybrid dysgenesis indicated otherwise. More recently, an analysis of transposition in the P element system indicated movement of elements other than the P element. Thus, it appears that co-mobilization may be a common feature of dysgenic syndromes.

What is the mechanism of co-mobilization? For the P element system, studies by William Theurkauf and colleagues point to the DNA damage response as key. Specifically, via Chk2 kinase, DNA damage signaling leads to perturbed piRNA biogenesis, which in turn leads to the activation of other elements under control of piRNA-based silencing. Does this mechanism also apply to other systems?

To study the mechanism of TE co-mobilization in the D. virilis system, we performed small RNA sequencing and mRNA sequencing experiments using germline material of reciprocal females of the dysgenic and non-dysgenic crosses. In contrast to the P element and I element systems, hybrid dysgenesis in D. virilis is more complex. For one, there is not a single element that has been proven to be the sole cause. This was previously shown, but in this study we identified several more elements that likely contribute. From small RNA sequencing, we find that TE mis-expression persists in the progeny of the dysgenic cross, without a persisting global defect in piRNA biogenesis. Rather, it appears that piRNA biogenesis defects are idiosyncratic across different TE families. Interestingly, we also find evidence that piRNA silencing loses specificity in the dysgenic cross, with some highly expressed genes becoming non-specific targets.

Overall, this study provided several insights, but the mechanism of co-mobilization in the D. virilis system remains unknown. The complexity of this syndrome makes it a challenge for study, but it may provide significant insight into genome dynamics of hybrids whose parents differ for more than one TE family. Future genetic analysis may allow us to determine the role of the DNA damage response in maintaining the activity of some TE families, but not others.