< i > Har-P < /i > , a short < i > P < /i > -element variant, weaponizes < i > P < /i > -transposase to severely impair < i > Drosophila < /i > development

Without transposon-silencing Piwi-interacting RNAs (piRNAs), transposition causes an ovarian atrophy syndrome inDrosophila called gonadal dysgenesis (GD).Harwich (Har) strains withP-elements cause severe GD in F1 daughters whenHar fathers mate with mothers lackingP-element-piRNAs (i.e.ISO1 strain). To address the mystery of whyHar induces severe GD, we bred hybridDrosophila withHar genomic fragments into theISO1 background to createHISR-D or HISR-N lines that still causeDysgenesis or areNon-dysgenic, respectively. In these lines, we discovered a highly truncatedP-element variant we named ‘Har-P’ as the most frequent de novo insertion. AlthoughHISR-D lines still contain full-lengthP-elements,HISR-N lines 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 ’s transmitted paternally to suppress somatic transposition. TheDrosophila shortHar-P ’s and full-lengthP-elements relationship parallels the MITEs/DNA-transposase in plants and SINEs/LINEs in mammals.
Source: eLife - Category: Biomedical Science Tags: Chromosomes and Gene Expression Genetics and Genomics Source Type: research