Whole genome sequencing in Drosophila virilis identifies Polyphemus, a recently activated Tc1-like transposon with a possible role in hybrid dysgenesis.

backgroundHybrid dysgenic syndromes in Drosophila have been critical for characterizing host mechanisms of transposable element (TE) regulation. This is because a common feature of hybrid dysgenesis is germline TE mobilization that occurs when paternally inherited TEs are not matched with a maternal pool of silencing RNAs that maintain transgenerational TE control. In the face of this imbalance TEs become activated in the germline and can cause F1 sterility. The syndrome of hybrid dysgenesis in Drosophila virilis was the first to show that the mobilization of one dominant TE, the Penelope retrotransposon, may lead to the mobilization of other unrelated elements. However, it is not known how many different elements contribute and no exhaustive search has been performed to identify additional ones. To identify additional TEs that may contribute to hybrid dysgenesis in Drosophila virilis, I analyzed repeat content in genome sequences of inducer and non-inducer lines.

resultsHere I describe Polyphemus, a novel Tc1-like DNA transposon, which is abundant in the inducer strain of D. virilis but highly degraded in the non-inducer strain. Polyphemus expression is also increased in the germline of progeny of the dysgenic cross relative to reciprocal progeny. Interestingly, like the Penelope element, it has experienced recent re-activation within the D. virilis lineage.

conclusionsHere I present the results of a comprehensive search to identify additional factors that may cause hybrid dysgenesis in D. virilis. Polyphemus, a novel Tc1-like DNA transposon, has recently become re-activated in Drosophila virilis and likely contributes to the hybrid dysgenesis syndrome. It has been previously shown that the Penelope element has also been re-activated in the inducer strain. This suggests that TE co-reactivation within species may synergistically contribute to syndromes of hybrid dysgenesis.