An RNA splicing system that excises DNA transposons from animal mRNAs

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. A new type of mRNA splicing mechanism discovered in Caenorhabditis elegans that detects and removes inverted repeats also occurs in human cells, thereby providing another strategy to protect against the negative effects of transposable elements.