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Elife. 2019 Dec 17;8. pii: e49948. doi: 10.7554/eLife.49948.

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

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Department of Biochemistry, Boston University School of Medicine, Boston University, Boston, United States.
Department of Biology, Brandeis University, Waltham, United States.
Genome Science Institute, Boston University School of Medicine, Boston, United States.


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.


D. melanogaster; P-element; chromosomes; gene expression; genetics; genomics; gonadal dysgenesis; piRNA; transposon silencing

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