Western blot for Vasa in control and dysgenic ovaries. Vasa also shows the expected accumulation at the posterior pole of stage 10 oocytes (right panels). At 21 days, by contrast, Vasa is present in the cytoplasm and nuage in both dysgenic hybrids and reciprocal control. At 2–4 days, only low levels of Vasa is present in the germarium of dysgenic hybrids (2–4 Day, w 1 × Har), while Vasa is dispersed in the cytoplasm and concentrated in perinuclear foci (nuage) in reciprocal hybrid controls (2–4 Day, Har × w 1). Vasa localization and expression during hybrid dysgenesis. P element invasion thus triggers heritable changes in genome structure that appear to enhance transposon silencing.Ĭopyright © 2011 Elsevier Inc. Significantly, resident transposons insert into piRNA clusters, and these new insertions are transmitted to progeny, produce novel piRNAs, and are associated with reduced transposition. ![]() In addition, the piRNA biogenesis machinery assembles, and resident elements are silenced. As dysgenic hybrids age, however, fertility is restored, P elements are silenced, and P element piRNAs are produced de novo. We show that P-M hybrid dysgenesis activates both P elements and resident transposons and disrupts the piRNA biogenesis machinery. Paternally inherited P element transposons thus escape silencing and trigger a hybrid sterility syndrome termed P-M hybrid dysgenesis. In Drosophila, piRNAs are encoded by heterochromatic clusters and maternally deposited in the embryo. Piwi-interacting RNAs (piRNAs) silence these genome pathogens, but it is unclear how the piRNA pathway adapts to invasion of new transposons. Transposons evolve rapidly and can mobilize and trigger genetic instability.
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