piRNA loss unleashes episodic transposition bursts
- 1Department of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853
- 2Harvard-Massachusetts Institute of Technology Program in Health Sciences and Technology, Harvard Medical School, Boston, MA 02115
Abstract
In Metazoa, transposon expression is suppressed by the piRNA pathway, and disruption of this pathway leads to rampant transposon expression. However, it remains unclear whether increased transposon expression results in actual transposition, and if so, which and how frequently transposons mobilize upon piRNA loss. Here, we developed a framework to track transposon copy accumulation across generations on a single set of nonrecombining haploid genome in the Drosophila male germline, with or without the piRNA biogenesis factor HP1D/Rhino. Single-fly Nanopore DNA sequencing revealed that multiple transposon families mobilized after 10 to 45 generations of piRNA loss. Among them, the most prolific across all replicates was copia, producing dozens of new insertions that were distributed across chromosome arms. With genomic DNA collected at every generation, we validated and dated each copia insertion, revealing episodic bursts of transposition that deviated strongly from a Poisson process. Using phylogenetic analysis, we further showed that multiple copia loci—both autonomous and nonautonomous copies—can mobilize. Interestingly, two additional transposon families, mdg3 and invader3, also mobilized episodically, but with distinct timing and magnitude, highlighting the stochastic nature of transposition bursts. Because we did not observe a single transposition event for these elements in controls, our results provide direct evidence that the piRNA pathway tightly suppresses germline transposition. More importantly, our findings argue that disruption of the piRNA pathway does not simply elevate transposition rates, but it instead unleashes punctuated and stochastic bursts of transposon movement that may radically reshape the timing and magnitude of mutational input during evolution.
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BibTeX
@article{chen2026pirna,
title = {{piRNA loss unleashes episodic transposition bursts}},
author = {Peiwei Chen and Peiyu Xu and Hamna Waseem and John McCormick and Katherine C. Pan and Alexei A. Aravin and Andrew G. Clark and Cédric Feschotte},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
year = {2026},
month = oct,
doi = {10.1073/pnas.2623866123},
url = {https://doi.org/10.1073/pnas.2623866123},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - piRNA loss unleashes episodic transposition bursts
AU - Peiwei Chen
AU - Peiyu Xu
AU - Hamna Waseem
AU - John McCormick
AU - Katherine C. Pan
AU - Alexei A. Aravin
AU - Andrew G. Clark
AU - Cédric Feschotte
PY - 2026
DA - 2026/10/28
JO - Proceedings of the National Academy of Sciences of the United States of America
DO - 10.1073/pnas.2623866123
UR - https://doi.org/10.1073/pnas.2623866123
AB - In Metazoa, transposon expression is suppressed by the piRNA pathway, and disruption of this pathway leads to rampant transposon expression. However, it remains unclear whether increased transposon expression results in actual transposition, and if so, which and how frequently transposons mobilize upon piRNA loss. Here, we developed a framework to track transposon copy accumulation across generations on a single set of nonrecombining haploid genome in the Drosophila male germline, with or without the piRNA biogenesis factor HP1D/Rhino. Single-fly Nanopore DNA sequencing revealed that multiple transposon families mobilized after 10 to 45 generations of piRNA loss. Among them, the most prolific across all replicates was copia, producing dozens of new insertions that were distributed across chromosome arms. With genomic DNA collected at every generation, we validated and dated each copia insertion, revealing episodic bursts of transposition that deviated strongly from a Poisson process. Using phylogenetic analysis, we further showed that multiple copia loci—both autonomous and nonautonomous copies—can mobilize. Interestingly, two additional transposon families, mdg3 and invader3, also mobilized episodically, but with distinct timing and magnitude, highlighting the stochastic nature of transposition bursts. Because we did not observe a single transposition event for these elements in controls, our results provide direct evidence that the piRNA pathway tightly suppresses germline transposition. More importantly, our findings argue that disruption of the piRNA pathway does not simply elevate transposition rates, but it instead unleashes punctuated and stochastic bursts of transposon movement that may radically reshape the timing and magnitude of mutational input during evolution.
SN - 0027-8424
SN - 1091-6490
ER -