Har-P, a short P-element variant, weaponizes P-transposase to severely impair Drosophila development

• DOI: 10.7554/elife.49948
• Publication Date: 2019-12-12T15:00:16Z
• Authors: Satyam P Srivastav; Reazur Rahman; Qicheng Ma; Jasmine Pierre; Saptaparni Bandyo...; Nelson C Lau
• Keywords: 0301 basic medicine; gonadal dysgenesis; QH301-705.5; Science; Q; Ovary; R; Gene Dosage; Pupa; Transposases; piRNA; Chromosomes and Gene Expression; 03 medical and health sciences; Drosophila melanogaster; Germ Cells; DNA Transposable Elements; P-element; transposon silencing; Medicine; Animals; Female; Gene Silencing; Biology (General); RNA, Small Interfering

Without transposon-silencing Piwi-interacting RNAs (piRNAs), transposition causes an ovarian atrophy syndrome in Drosophila called gonadal dysgenesis (GD). Harwich (Har) strains with P-elements cause severe GD in F1 daughters when Har fathers mate with mothers lacking P-element-piRNAs (i.e. ISO1 strain). To address the mystery of why Har induces severe GD, we bred hybrid Drosophila with Har genomic fragments into the ISO1 background to create HISR-D or HISR-N lines that still cause Dysgenesis or are Non-dysgenic, respectively. In these lines, we discovered a highly truncated P-element variant we named ‘Har-P’ as the most frequent de novo insertion. Although HISR-D lines still contain full-length P-elements, HISR-N lines lost functional P-transposase but retained Har-P’s that when crossed back to P-transposase restores GD induction. Finally, we uncovered P-element-piRNA-directed repression on Har-P’s transmitted paternally to suppress somatic transposition. The Drosophila short Har-P’s and full-length P-elements relationship parallels the MITEs/DNA-transposase in plants and SINEs/LINEs in mammals.