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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.

Author information

1
Department of Biochemistry, Boston University School of Medicine, Boston University, Boston, United States.
2
Department of Biology, Brandeis University, Waltham, United States.
3
Genome Science Institute, Boston University School of Medicine, Boston, United States.

Abstract

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.

KEYWORDS:

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

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