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bioRxiv · 10.1101/2025.10.13.681963

Flamenco plasticity tunes somatic piRNAs, rewiring host isoforms and opening a route to heritable transposon spread

Moritoh, M.·Takeuchi, C.·Namba, Y.·Nishihara, H.·Hirakata, S.·Owa, C.·Moritshita, S.·Iwasaki, Y. W.·Siomi, M. C.
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Abstract

Transposons drive genome innovation, yet how they evade somatic piRNA defenses, reach the germline, and rewire host genes with limited cost remains unclear. Using comparative long-read sequencing in Drosophila ovarian somatic cells (OSCs), we show that the LTR transposon Springer rewires gene expression by inserting into promoter-proximal introns at an AT-rich motif. Its 5' LTR initiates transcripts that splice into host exons, expanding isoform diversity without adding coding sequence. We catalog 72 Springer-driven isoforms, indicating broad mutagenic potential. In parallel, the Flamenco (Flam) uni-strand piRNA cluster undergoes structural remodeling that replaces antisense transposon fragments with forward-oriented copies, reshaping piRNA populations and eroding silencing of specific elements, including Springer. This relaxation of somatic repression creates conditions permissive for germ-cell entry, providing a plausible route to heritable genome change. Thus, Flam plasticity, contrasting with the relative stability of dual-strand clusters, mechanistically links transposon activity to genome rewiring and evolutionary innovation.

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Moritoh, M., Takeuchi, C., Namba, Y., Nishihara, H., Hirakata, S., Owa, C., Moritshita, S., Iwasaki, Y. W., Siomi, M. C.. 2025-10-14. Flamenco plasticity tunes somatic piRNAs, rewiring host isoforms and opening a route to heritable transposon spread. https://doi.org/10.1101/2025.10.13.681963

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