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dc.contributor.authorHemmer, Lucas W.
dc.contributor.authorDias, Guilherme B.
dc.contributor.authorSmith, Brittny
dc.contributor.authorVaerenberghe, Kelley Van
dc.contributor.authorHoward, Ashley
dc.contributor.authorBergman, Casey M.
dc.contributor.authorBlumenstiel, Justin P.
dc.date.accessioned2020-06-16T18:17:43Z
dc.date.available2020-06-16T18:17:43Z
dc.date.issued2020-02-15
dc.identifier.citationHemmer, L. W., Dias, G. B., Smith, B., Van Vaerenberghe, K., Howard, A., Bergman, C. M., & Blumenstiel, J. P. (2020). Hybrid dysgenesis in Drosophila virilis results in clusters of mitotic recombination and loss-of-heterozygosity but leaves meiotic recombination unaltered. Mobile DNA, 11, 10. https://doi.org/10.1186/s13100-020-0205-0en_US
dc.identifier.urihttp://hdl.handle.net/1808/30508
dc.descriptionThis work is licensed under a Creative Commons Attribution 4.0 International License.en_US
dc.description.abstractBackground 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.
en_US
dc.publisherBMCen_US
dc.rights© The Author(s) 2020.en_US
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en_US
dc.subjectDrosophila virilisen_US
dc.subjectHybrid dysgenesisen_US
dc.subjectTransposonsen_US
dc.subjectMeiotic recombinationen_US
dc.subjectMitotic recombinationen_US
dc.titleHybrid dysgenesis in Drosophila virilis results in clusters of mitotic recombination and loss-of-heterozygosity but leaves meiotic recombination unaltereden_US
dc.typeArticleen_US
kusw.kuauthorHemmer, Lucas W.
kusw.kuauthorSmith, Brittny
kusw.kuauthorVaerenberghe, Kelley Van
kusw.kuauthorHoward, Ashley
kusw.kuauthorBlumenstiel, Justin P.
kusw.kudepartmentEcology and Evolutionary Biologyen_US
kusw.kudepartmentMolecular Biosciencesen_US
dc.identifier.doi10.1186/s13100-020-0205-0en_US
dc.identifier.orcidhttps://orcid.org/0000-0002-8036-5207en_US
kusw.oaversionScholarly/refereed, publisher versionen_US
kusw.oapolicyThis item meets KU Open Access policy criteria.en_US
dc.identifier.pmidPMC7023781en_US
dc.rights.accessrightsopenAccessen_US


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Except where otherwise noted, this item's license is described as: © The Author(s) 2020.