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dc.contributor.authorFunikov, Sergei Y.
dc.contributor.authorKulikova, Dina A.
dc.contributor.authorKrasnov, George S.
dc.contributor.authorRezvykh, Alexander P.
dc.contributor.authorChuvakova, Lubov N.
dc.contributor.authorShostak, Natalia G.
dc.contributor.authorZelentsova, Elena S.
dc.contributor.authorBlumenstiel, Justin P.
dc.contributor.authorEvgen'ev, Michael B.
dc.date.accessioned2018-09-20T19:14:03Z
dc.date.available2018-09-20T19:14:03Z
dc.date.issued2018-05-29
dc.identifier.citationFunikov SY, Kulikova DA, Krasnov GS, Rezvykh AP, Chuvakova LN, Shostak NG, et al. (2018) Spontaneous gain of susceptibility suggests a novel mechanism of resistance to hybrid dysgenesis in Drosophila virilis. PLoS Genet 14(5): e1007400. https://doi.org/10.1371/journal.pgen.1007400en_US
dc.identifier.urihttp://hdl.handle.net/1808/26745
dc.description.abstractSyndromes of hybrid dysgenesis (HD) have been critical for our understanding of the transgenerational maintenance of genome stability by piRNA. HD in D. virilis represents a special case of HD since it includes simultaneous mobilization of a set of TEs that belong to different classes. The standard explanation for HD is that eggs of the responder strains lack an abundant pool of piRNAs corresponding to the asymmetric TE families transmitted solely by sperm. However, there are several strains of D. virilis that lack asymmetric TEs, but exhibit a “neutral” cytotype that confers resistance to HD. To characterize the mechanism of resistance to HD, we performed a comparative analysis of the landscape of ovarian small RNAs in strains that vary in their resistance to HD mediated sterility. We demonstrate that resistance to HD cannot be solely explained by a maternal piRNA pool that matches the assemblage of TEs that likely cause HD. In support of this, we have witnessed a cytotype shift from neutral (N) to susceptible (M) in a strain devoid of all major TEs implicated in HD. This shift occurred in the absence of significant change in TE copy number and expression of piRNAs homologous to asymmetric TEs. Instead, this shift is associated with a change in the chromatin profile of repeat sequences unlikely to be causative of paternal induction. Overall, our data suggest that resistance to TE-mediated sterility during HD may be achieved by mechanisms that are distinct from the canonical syndromes of HD.en_US
dc.publisherPublic Library of Scienceen_US
dc.rights© 2018 Funikov et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/en_US
dc.titleSpontaneous gain of susceptibility suggests a novel mechanism of resistance to hybrid dysgenesis in Drosophila virilisen_US
dc.typeArticleen_US
kusw.kuauthorBlumenstiel, Justin P.
kusw.kudepartmentCenter for Computational Biologyen_US
dc.identifier.doi10.1371/journal.pgen.1007400en_US
kusw.oaversionScholarly/refereed, publisher versionen_US
kusw.oapolicyThis item meets KU Open Access policy criteria.en_US
dc.rights.accessrightsopenAccessen_US


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© 2018 Funikov et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Except where otherwise noted, this item's license is described as: © 2018 Funikov et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.