ArticleRNA (New York, N.Y.)2012
Post-transcriptional modification of spliceosomal RNAs is normal in SMN-deficient cells.
Article in RNA (New York, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 41 citations in OpenAlex.
- Deciphering the pseudouridine nucleobase modification in human diseases: From molecular mechanisms to clinical perspectives.Clinical and translational medicine · 2025Review
- An integrative platform for detection of RNA 2'-O-methylation reveals its broad distribution on mRNA.Cell reports methods · 2024Article
- PanCancer analysis of somatic mutations in repetitive regions reveals recurrent mutations in snRNA U2.NPJ genomic medicine · 2022Article
- Ribosomal RNA Pseudouridylation: Will Newly Available Methods Finally Define the Contribution of This Modification to Human Ribosome Plasticity?Frontiers in genetics · 2022Review
- SnoRNA guide activities: real and ambiguous.RNA (New York, N.Y.) · 2021Article
- Small but Mighty-The Emerging Role of snoRNAs in Hematological Malignancies.Non-coding RNA · 2021Review
- The small Cajal body-specific RNA 15 (SCARNA15) directs p53 and redox homeostasis via selective splicing in cancer cells.NAR cancer · 2021Article
- Nopp140-chaperoned 2'-O-methylation of small nuclear RNAs in Cajal bodies ensures splicing fidelity.Genes & development · 2021Article
- Spliceosomal snRNA Epitranscriptomics.Frontiers in genetics · 2021Review
- Regulation and Function of RNA Pseudouridylation in Human Cells.Annual review of genetics · 2020Review
- Synergistic interactions between Cajal bodies and the miRNA processing machinery.Molecular biology of the cell · 2020Article
- "Lost and Found": snoRNA Annotation in the Xenopus Genome and Implications for Evolutionary Studies.Molecular biology and evolution · 2020Article
- Identification of U11snRNA as an endogenous agonist of TLR7-mediated immune pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Small, Smaller, Smallest: Minimal Structural Requirements for a Fully Functional Box C/D Modification Guide RNA.Biomolecules · 2019Article
- The Epitranscriptome in Translation Regulation.Cold Spring Harbor perspectives in biology · 2019Review
- Beyond rRNA and snRNA: tRNA as a 2'-O-methylation target for nucleolar and Cajal body box C/D RNPs.Genes & development · 2019Article
- Cooperative 2'-O-methylation of the wobble cytidine of human elongator tRNAGenes & development · 2019Article
- TDP-43 regulates site-specific 2'-O-methylation of U1 and U2 snRNAs via controlling the Cajal body localization of a subset of C/D scaRNAs.Nucleic acids research · 2019Article
- Biology and clinical relevance of noncoding sno/scaRNAs.Trends in cardiovascular medicine · 2018Review
- Orchestrated positioning of post-transcriptional modifications at the branch point recognition region of U2 snRNA.RNA (New York, N.Y.) · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The survival of motor neuron (SMN) protein plays an important role in the biogenesis of spliceosomal snRNPs and is one factor required for the integrity of nuclear Cajal bodies (CBs). CBs are enriched in small CB-specific (sca) RNAs, which guide the formation of pseudouridylated and 2'-O-methylated residues in the snRNAs. Because SMN-deficient cells lack typical CBs, we asked whether the modification of internal residues of major and minor snRNAs is defective in these cells. We mapped modified nucleotides in the major U2 and the minor U4atac and U12 snRNAs. Using both radioactive and fluorescent primer extension approaches, we found that modification of major and minor spliceosomal snRNAs is normal in SMN-deficient cells. Our experiments also revealed a previously undetected pseudouridine at position 60 in human U2 and 2'-O-methylation of A1, A2, and G19 in human U4atac. These results confirm, and extend to minor snRNAs, previous experiments showing that scaRNPs can function in the absence of typical CBs. Furthermore, they show that the differential splicing defects in SMN-deficient cells are not due to failure of post-transcriptional modification of either major or minor snRNAs.
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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.