ArticleeLife2022
Type I and II PRMTs inversely regulate post-transcriptional intron detention through Sm and CHTOP methylation.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Identification and Validation of Key Genes Related to Arginine Methylation Modification in Sepsis Using Transcriptome Combined with Mendelian Randomization Analysis.Shock (Augusta, Ga.) · 2026Article
- Pharmacological perturbation of splicing elicits SMG1 reduction: Implications for cancer therapy.iScience · 2026Article
- PRMT5 inhibitors actively promote metastatic progression of lung adenocarcinoma.bioRxiv : the preprint server for biology · 2026Article
- Protein arginine methyltransferases in protozoan parasites: a new path for antiparasitic chemotherapy?Microbial cell (Graz, Austria) · 2026Article
- Unraveling the FGFR-RNA splicing axis: Mechanisms, oncogenic crosstalks and innovations for therapeutic purpose.Acta pharmaceutica Sinica. B · 2026Review
- Productive mRNA chromatin escape is promoted by PRMT5 activity.Molecular cell · 2025Article
- PRMT5 activity sustains histone production to maintain genome integrity.bioRxiv : the preprint server for biology · 2025Article
- The regulation and function of post-transcriptional RNA splicing.Nature reviews. Genetics · 2025Review
- PRMT5 promotes full-length HTT expression by repressing multiple proximal intronic polyadenylation sites.Nucleic acids research · 2025Article
- PRMT5-regulated splicing of DNA repair genes drives chemoresistance in breast cancer stem cells.Oncogene · 2025Article
- Nuclear mRNA decay: regulatory networks that control gene expression.Nature reviews. Genetics · 2024Review
- Article
- PRMT2 silencing regulates macrophage polarization through activation of STAT1 or inhibition of STAT6.BMC immunology · 2024Article
- Research Progress on the Role of Epigenetic Methylation Modification in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2024Review
- Review
- Tudor-dimethylarginine interactions: the condensed version.Trends in biochemical sciences · 2023Review
- Effectors and effects of arginine methylation.Biochemical Society transactions · 2023Article
- Review
- Regulation of Pre-mRNA Splicing: Indispensable Role of Post-Translational Modifications of Splicing Factors.Life (Basel, Switzerland) · 2023Review
- Competing Endogenous RNA (ceRNA) Networks and Splicing Switches in Cervical Cancer: HPV Oncogenesis, Clinical Significance and Therapeutic Opportunities.Microorganisms · 2022Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Protein arginine methyltransferases (PRMTs) are required for the regulation of RNA processing factors. Type I PRMT enzymes catalyze mono- and asymmetric dimethylation; Type II enzymes catalyze mono- and symmetric dimethylation. To understand the specific mechanisms of PRMT activity in splicing regulation, we inhibited Type I and II PRMTs and probed their transcriptomic consequences. Using the newly developed Splicing Kinetics and Transcript Elongation Rates by Sequencing (SKaTER-seq) method, analysis of co-transcriptional splicing demonstrated that PRMT inhibition resulted in altered splicing rates. Surprisingly, co-transcriptional splicing kinetics did not correlate with final changes in splicing of polyadenylated RNA. This was particularly true for retained introns (RI). By using actinomycin D to inhibit ongoing transcription, we determined that PRMTs post-transcriptionally regulate RI. Subsequent proteomic analysis of both PRMT-inhibited chromatin and chromatin-associated polyadenylated RNA identified altered binding of many proteins, including the Type I substrate, CHTOP, and the Type II substrate, SmB. Targeted mutagenesis of all methylarginine sites in SmD3, SmB, and SmD1 recapitulated splicing changes seen with Type II PRMT inhibition, without disrupting snRNP assembly. Similarly, mutagenesis of all methylarginine sites in CHTOP recapitulated the splicing changes seen with Type I PRMT inhibition. Examination of subcellular fractions further revealed that RI were enriched in the nucleoplasm and chromatin. Taken together, these data demonstrate that, through Sm and CHTOP arginine methylation, PRMTs regulate the post-transcriptional processing of nuclear, detained introns.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.