An RNA splicing system that excises DNA transposons from animal mRNAs.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 41372403.
- Also identified by DOI 10.1038/s41586-025-09853-8 and PMC identifier 12779559.
- Licence recorded as CC BY-NC-ND.
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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.
Medical subject headings
- RNA Splicing
- Caenorhabditis elegans
- RNA, Messenger
- DNA Transposable Elements