ArticleThe Journal of biological chemistry2023
The U1 antisense morpholino oligonucleotide (AMO) disrupts U1 snRNP structure to promote intronic PCPA modification of pre-mRNAs.
Article in The Journal of biological chemistry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Alternative Splicing: Molecular Mechanisms, Biological Functions, Diseases, and Potential Therapeutic Targets.MedComm · 2025Review
- RNA polymerase III transcription-associated polyadenylation promotes the accumulation of noncoding retrotransposons during infection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Therapeutic targeting of RNA for neurological and neuromuscular disease.Genes & development · 2024Review
- U4 snRNP inhibits premature cleavage and polyadenylation of pre-mRNAs.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Transcription elongation defects link oncogenic SF3B1 mutations to targetable alterations in chromatin landscape.Molecular cell · 2024Article
- InPACT: a computational method for accurate characterization of intronic polyadenylation from RNA sequencing data.Nature communications · 2024Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
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Abstract
Functional depletion of the U1 small nuclear ribonucleoprotein (snRNP) with a 25 nt U1 AMO (antisense morpholino oligonucleotide) may lead to intronic premature cleavage and polyadenylation of thousands of genes, a phenomenon known as U1 snRNP telescripting; however, the underlying mechanism remains elusive. In this study, we demonstrated that U1 AMO could disrupt U1 snRNP structure both in vitro and in vivo, thereby affecting the U1 snRNP-RNAP polymerase II interaction. By performing chromatin immunoprecipitation sequencing for phosphorylation of Ser2 and Ser5 of the C-terminal domain of RPB1, the largest subunit of RNAP polymerase II, we showed that transcription elongation was disturbed upon U1 AMO treatment, with a particular high phosphorylation of Ser2 signal at intronic cryptic polyadenylation sites (PASs). In addition, we showed that core 3'processing factors CPSF/CstF are involved in the processing of intronic cryptic PAS. Their recruitment accumulated toward cryptic PASs upon U1 AMO treatment, as indicated by chromatin immunoprecipitation sequencing and individual-nucleotide resolution CrossLinking and ImmunoPrecipitation sequencing analysis. Conclusively, our data suggest that disruption of U1 snRNP structure mediated by U1 AMO provides a key for understanding the U1 telescripting mechanism.
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