Abstract

All genomes have mobile genetic segments called transposable elements (TEs)<sup>1</sup>. Here we describe a system, which we term SOS splicing, that protects Caenorhabditis elegans and human genes against DNA-transposon-mediated disruption by excising these TEs from host mRNAs. SOS splicing, which seems to operate independently of the spliceosome, is a pattern-recognition system triggered by the base-pairing of inverted terminal repeat elements, which are a defining feature of DNA transposons. We identify three factors required for SOS splicing in both C. elegans and human cells: AKAP17A, which binds TE-containing mRNAs; the RNA ligase RTCB; and CAAP1, which bridges RTCB and AKAP17A to allow RTCB to ligate mRNA fragments generated by TE excision. We propose that SOS splicing is a previously undescribed conserved and RNA-structure-directed mode of mRNA splicing, and that an identified function of SOS splicing is to genetically buffer animals from the deleterious effects of DNA-transposon-mediated gene perturbation.

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Year
2025
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article
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1
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Long‐Wen Zhao, Christopher Nardone, Cindy Chang et al. (2025). An RNA splicing system that excises DNA transposons from animal mRNAs. Nature . https://doi.org/10.1038/s41586-025-09853-8

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DOI
10.1038/s41586-025-09853-8