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An RNA Splicing System that Excises DNA Transposons from Animal mRNAs [Illlumina]

ABSTRACT: All genomes harbor mobile genetic parasites called transposable elements (TEs). Here we describe a system, which we term SOS splicing, that protects C. elegans and human genes from DNA transposon-mediated disruption by excising these TEs from host mRNAs. SOS splicing, which appears to operate independently of the spliceosome, is a pattern recognition system triggered by 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, allowing RTCB to ligate mRNA fragments generated by TE excision. We propose that SOS splicing is a novel, conserved, and RNA structure-directed mode of mRNA splicing and that one function of SOS splicing is to genetically buffer animals from the deleterious effects of DNA-transposon-mediated gene perturbation.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE288885 | GEO | 2025/09/17

REPOSITORIES: GEO

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An RNA Splicing System that Excises DNA Transposons from Animal mRNAs

Project description:All genomes harbor mobile genetic parasites called transposable elements (TEs). Here we describe a system, which we term SOS splicing, that protects C. elegans and human genes from DNA transposon-mediated disruption by excising these TEs from host mRNAs. SOS splicing, which operates independently of the spliceosome, is a pattern recognition system triggered by base- pairing of inverted terminal repeat elements, which are a defining feature of the 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, allowing RTCB to ligate mRNA fragments generated by TE excision. We propose that SOS splicing is a novel, conserved, and RNA structure-directed mode of mRNA splicing and that one function of SOS splicing is to genetically buffer animals from the deleterious effects of TE- mediated gene perturbation.

2025-09-22 | PXD068578 | Pride

An RNA Splicing System that Excises DNA Transposons from Animal mRNAs [Nanopore]

Project description:All genomes harbor mobile genetic parasites called transposable elements (TEs). Here we describe a system, which we term SOS splicing, that protects C. elegans and human genes from DNA transposon-mediated disruption by excising these TEs from host mRNAs. SOS splicing, which appears to operate independently of the spliceosome, is a pattern recognition system triggered by 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, allowing RTCB to ligate mRNA fragments generated by TE excision. We propose that SOS splicing is a novel, conserved, and RNA structure-directed mode of mRNA splicing and that one function of SOS splicing is to genetically buffer animals from the deleterious effects of DNA-transposon-mediated gene perturbation.

2025-09-17 | GSE288884 | GEO

TDP-43 dysfunction leads to the accumulation of cryptic transposable element-derived exons in iPSC derived neurons and ALS/FTD patient tissues [brain isoseq]

Project description:TDP-43 is an RNA and DNA binding protein that plays major roles in regulating RNA processing. In particular, TDP-43 dysfunction leads to the accumulation of cryptic splice isoforms that result from improperly spliced mRNAs. In addition to its role in regulating splicing, TDP-43 is also known to regulate the expression of transposable elements (TEs). TEs are mobile genetic elements which comprise a significant proportion of the human genome, but are normally silenced in healthy somatic cells. TEs are interspersed throughout the genome, both in gene-depleted regions and interspersed within gene introns and gene regulatory sequences. We used optimized long-read RNA sequencing assays to generate catalogs of mis-spliced and mis-expressed genes and TEs in human neurons depleted for TDP-43. In addition to known TDP-43 driven cryptic isoforms, we identified hundreds of TDP-43 dependent spliced RNAs formed as part of cryptic gene-TE fusion events that result from mis-splicing of TE sequences into gene transcripts. Among these TDP-43 dependent gene-TE cryptic transcripts (crypTEs), we found: TEs that provide alternate gene promoters/5’UTRs, TEs that act as cassette exons inside host gene mRNAs, as well as TEs that provide alternate transcript 3’ ends. These cryptic gene-TE fusions are predicted to induce: aberrant expression of ALS relevant genes, nonsense mediated decay (NMD) products, as well as novel peptides from gene-TE fusions within the gene coding sequence. We further verified that many of these crypTE transcripts are detected in ALS/FTD cortical tissues with TDP-43 pathology. In short, TDP-43 dependent CrypTE events represent a large reservoir of ALS/FTD relevant transcripts and peptides that are not captured by standard assays and analyses.

2026-01-09 | GSE315972 | GEO

TDP-43 dysfunction leads to the accumulation of cryptic transposable element-derived exons in iPSC derived neurons and ALS/FTD patient tissues [i3N isoseq]

2026-01-09 | GSE310723 | GEO

TDP-43 dysfunction leads to the accumulation of cryptic transposable element-derived exons in iPSC derived neurons and ALS/FTD patient tissues [i3N RNAseq]

2026-01-09 | GSE310722 | GEO

RNA Ligase RTCB-mediated mRNA Alternative Splicing is Required for Mouse Oocyte Development and Maintenance

Project description:Intron splicing of the pre-mRNA is usually coupled with the transcription elongation catalyzed by RNA polymerase. However, recent large-scale mRNA sequencing showed that introns are still retained in 5-10% of mRNA, these introns are named as exitrons. They are deleted in some special cells or conditions to deal with developmental transition or cellular stress response. The role of this mechanism in mammalian female reproduction is elusive so far. We found that RNA terminal phosphate cyclase B (RTCB) mainly regulated splicing of these transcripts related to p-CDK1, DNA methylation and DNA damage repair. On the one hand, it regulated the recovery of oocyte meiosis by affecting CDK1 activation. On the other hand, it also regulated the developmental potential of oocytes by influencing splicing of DNA methylation and DNA damage repair-related mRNA. In addition, it could also play a crucial role in follicular development. Rtcb deletion resulted in the accumulation of these maternal mRNAs containing unspliced introns, and the decline of the overall level of transcripts. As a result, Rtcb-/- female are sterile. Our study highlights the important role of RTCB-regulated non-canonical alternative splicing in female reproduction.

2022-10-10 | GSE190681 | GEO

The RtcB RNA ligase is an essential component of the metazoan unfolded protein response.

Project description:RNA ligation can regulate RNA function by altering RNA sequence, structure and coding potential. For example, the function of XBP1 in mediating the unfolded protein response requires RNA ligation, as does the maturation of some tRNAs. Here, we describe a novel in vivo model in C. elegans for the conserved RNA ligase RtcB, and show that RtcB ligates the xbp 1 mRNA during the IRE 1 branch of the unfolded protein response. Without RtcB, protein stress results in the accumulation of unligated xbp-1 mRNA fragments, defects in the unfolded protein response, and decreased lifespan. RtcB also ligates endogenous pre tRNA halves, and RtcB mutants have defects in growth and lifespan that can be bypassed by expression of pre-spliced tRNAs. In addition, animals that lack RtcB have defects that are independent of tRNA maturation and the unfolded protein response. Thus, RNA ligation by RtcB is required for the function of multiple endogenous target RNAs including both xbp-1 and tRNAs. RtcB is uniquely capable of performing these ligation functions, and RNA ligation by RtcB mediates multiple essential processes in vivo. 4 paired-end RNA-seq reads. Control worms have pre-spliced tRNAs, RtcB-null have mutated RtcB, +/- tunicamycin treatment

2014-09-24 | E-GEOD-61733 | biostudies-arrayexpress

Altered TE-derived genes leads to pathogenesis of FXD [ShortReadRNASeq]

Project description:We identified known and unknown transposon elements in the cells from healthy donors, FXD patients, and ALL patients by long-read RNA-sequencing. Using these identified TEs, we analyzed the expression of TE-derived genes by shot-read (illumina) RNA-sequencing. We found that expression of some specific TE-derived genes were changed in FXD compared to those in healthy donors. These findings suggested the involvement of modified expressions of TE-derived genes in the pathogenesis of FXD.

2024-10-30 | GSE264090 | GEO

Altered TE-derived genes leads to pathogenesis of FXD [PacBioRNASeq]

2024-10-30 | GSE264089 | GEO

Pervasive transcription and endosiRNAs restrain transposons during global demethylation in embryonic stem cells [smallRNA-Seq 2]

Project description:DNA methylation and other repressive epigenetic marks are erased in the mammalian germline and transposable elements (TEs) acquire the potential to be transcribed. This is a critical phase for genome defense and complementary TE silencing pathways are required to limit their activity. We find overlapping sense/antisense transcription in TEs in mouse embryonic stem cells, with an increase of sense transcription induced by acute deletion of Dnmt1, leading to increased abundance of small RNAs. These small RNAs are loaded into ARGONAUTE2 (AGO2) suggesting an endosiRNA based silencing mechanism. Reduction of Dicer and Ago2 levels reveals that small RNAs are involved in an immediate response to transposon activation by demethylation, while the deposition of repressive histone marks represents an ensuing chronic response. Dicer dependent endosiRNAs which map to TEs are also found in vivo during primordial germ cell development. Our results suggest that TE antisense transcription acts as a trap that restrains acute transposon activity through small RNAs during epigenetic reprogramming in the germline.

2017-11-01 | GSE102447 | GEO

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