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.
© 2019, Srivastav et al.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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DNA Transposable Elements / genetics*
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Drosophila melanogaster / genetics*
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Drosophila melanogaster / growth & development*
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Female
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Gene Dosage
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Gene Silencing
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Germ Cells / metabolism
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Ovary / metabolism
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Pupa / genetics
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RNA, Small Interfering / genetics
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Transposases / metabolism*
Substances
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DNA Transposable Elements
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RNA, Small Interfering
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Transposases