Background Transposable elements (TEs) are endogenous mutagens and their harmful effects are especially evident in syndromes of hybrid dysgenesis. In Drosophila virilis, hybrid dysgenesis is a syndrome of incomplete gonadal atrophy that occurs when males with multiple active TE families fertilize females that lack active copies of the same families. This has been demonstrated to cause the transposition of paternally inherited TE families, with gonadal atrophy driven by the death of germline stem cells. Because there are abundant, active TEs in the male inducer genome, that are not present in the female reactive genome, the D. virilis syndrome serves as an excellent model for understanding the effects of hybridization between individuals with asymmetric TE profiles. Results Using the D. virilis syndrome of hybrid dysgenesis as a model, we sought to determine how the landscape of germline recombination is affected by parental TE asymmetry. Using a genotyping-by-sequencing approach, we generated a high-resolution genetic map of D. virilis and show that recombination rate and TE density are negatively correlated in this species. We then contrast recombination events in the germline of dysgenic versus non-dysgenic F1 females to show that the landscape of meiotic recombination is hardly perturbed during hybrid dysgenesis. In contrast, hybrid dysgenesis in the female germline increases transmission of chromosomes with mitotic recombination. Using a de novo PacBio assembly of the D. virilis inducer genome we show that clusters of mitotic recombination events in dysgenic females are associated with genomic regions with transposons implicated in hybrid dysgenesis. Conclusions Overall, we conclude that increased mitotic recombination is likely the result of early TE activation in dysgenic progeny, but a stable landscape of meiotic recombination indicates that either transposition is ameliorated in the adult female germline or that regulation of meiotic recombination is robust to ongoing transposition. These results indicate that the effects of parental TE asymmetry on recombination are likely sensitive to the timing of transposition.

中文翻译：

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果蝇的杂交发育不全导致有丝分裂重组簇和杂合性丧失，但减数分裂重组保持不变。

背景转座因子 (TE) 是内源性诱变剂，其有害影响在杂种发育不全综合征中尤为明显。在绿色果蝇中，杂种发育不全是一种性腺不完全萎缩综合征，当具有多个活跃 TE 家族的雄性与缺乏同一家族活跃拷贝的雌性受精时，就会发生这种综合征。这已被证明会导致父系遗传的 TE 家族的转座，生殖干细胞死亡会导致性腺萎缩。因为雄性诱导基因组中有丰富的活性 TE，而雌性反应基因组中不存在，所以 D. virilis 综合征可作为了解具有不对称 TE 谱的个体之间杂交影响的极好模型。结果 以杂交不育的 D. virilis 综合征为模型，我们试图确定亲本 TE 不对称性如何影响种系重组的情况。使用测序方法进行基因分型，我们生成了 D. virilis 的高分辨率遗传图谱，并显示重组率和 TE 密度在该物种中呈负相关。然后，我们对比了发育不全与非发育不全的 F1 雌性生殖系中的重组事件，以表明减数分裂重组的景观在杂交发育不全期间几乎不受干扰。相反，雌性种系中的杂种发育不全通过有丝分裂重组增加了染色体的传递。使用 D. virilis 诱导基因组的从头 PacBio 组装，我们显示发育不全的雌性中的有丝分裂重组事件簇与基因组区域相关，其中转座子涉及杂种发育不全。结论 总体而言，我们得出结论，有丝分裂重组增加可能是发育不全后代早期 TE 激活的结果，但减数分裂重组的稳定景观表明，成年雌性生殖系中的转座或减数分裂重组的调节对正在进行的转座是稳健的。这些结果表明，亲本 TE 不对称对重组的影响可能对转座时间敏感。