Har-P, ashortP-element variant, weaponizesP-transposase to severely impairDrosophiladevelopment

Abstract

ABSTRACTWithout transposon-silencing Piwi-interacting RNAs (piRNAs), transposition causes an ovarian atrophy syndrome inDrosophilacalled gonadal dysgenesis (GD).Harwich(Har) strains withP-elements cause severe GD in F1 daughters whenHarfathers mate with mothers lackingP-element-piRNAs (i.e.ISO1strain). To address the mystery of whyHarinduces severe GD, we bred hybridDrosophilawithHargenomic fragments into theISO1background to createHISR-D or HISR-Nlines that still causeDysgenesis or areNon-dysgenic, respectively. In these lines, we discovered a highly truncatedP-element variant we named “Har-P” as the most frequentde novoinsertion. AlthoughHISR-Dlines still contain full-lengthP-elements,HISR-Nlines lost functionalP-transposase but retainedHar-P’s that when crossed back toP-transposase restores GD induction. Finally, we uncoveredP-element-piRNA-directed repression onHar-P’stransmitted paternally to suppress somatic transposition. TheDrosophilashortHar-P’sand full-lengthP-elements relationship parallels the MITEs/DNA-transposase in plants and SINEs/LINEs in mammals.