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-transposases in plants and SINEs/LINEs in mammals.

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