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December 10, 2025Nature1 citationsOpen Access

An RNA splicing system that excises DNA transposons from animal mRNAs

LZLong‐Wen ZhaoHarvard University CNChristopher NardoneBrigham and Women's Hospital CCCindy ChangHarvard University

Key Points

To describe a new RNA splicing system that excises DNA transposons from animal mRNAs to protect gene integrity.
Identified factors necessary for SOS splicing in C. elegans and human cells.
Investigated the role of AKAP17A, RTCB, and CAAP1 in the splicing process.
Examined how SOS splicing operates independently of the traditional spliceosome.
Demonstrated that the SOS splicing system excises DNA transposons from mRNAs.
Showed that SOS splicing is influenced by inverted terminal repeat elements.
Proposed that SOS splicing serves as a genetic buffer against transposon-mediated disruptions.

Abstract

All genomes have mobile genetic segments called transposable elements (TEs)1. 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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