ArticlePLoS genetics2015
Canonical Poly(A) Polymerase Activity Promotes the Decay of a Wide Variety of Mammalian Nuclear RNAs.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 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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Who cites it
81 citing papers in PubMed, 118 citations in OpenAlex.
- Review
- Efficient co-transcriptional splicing enforces rapid microexon definition and inclusion by SRRM4.bioRxiv : the preprint server for biology · 2026Article
- A kinetic ruler controls mRNA poly(A) tail length.Genes & development · 2025Article
- The regulation and function of post-transcriptional RNA splicing.Nature reviews. Genetics · 2025Review
- Genetic regulation of nascent RNA maturation revealed by direct RNA nanopore sequencing.Genome research · 2025Article
- The transcriptional and translational landscape of HCoV-OC43 infection.PLoS pathogens · 2025Article
- RNA 3'end tailing safeguards cells against products of pervasive transcription termination.Nature communications · 2024Article
- Nuclear mRNA decay: regulatory networks that control gene expression.Nature reviews. Genetics · 2024Review
- Modulation of mProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Phosphorylation of the nuclear poly(A) binding protein (PABPN1) during mitosis protects mRNA from hyperadenylation and maintains transcriptome dynamics.Nucleic acids research · 2024Article
- Genetic regulation of nascent RNA maturation revealed by direct RNA nanopore sequencing.bioRxiv : the preprint server for biology · 2024Article
- DEAD-box ATPase Dbp2 is the key enzyme in an mRNP assembly checkpoint at the 3'-end of genes and involved in the recycling of cleavage factors.Nature communications · 2024Article
- Genome-wide quantification of RNA flow across subcellular compartments reveals determinants of the mammalian transcript life cycle.Molecular cell · 2024Article
- Nuclear export is a limiting factor in eukaryotic mRNA metabolism.PLoS computational biology · 2024Article
- Fission yeast poly(A) polymerase active site mutation Y86D alleviates theRNA (New York, N.Y.) · 2023Article
- Functional analysis of 3'-UTR hairpins supports a two-tiered model for posttranscriptional regulation ofRNA (New York, N.Y.) · 2023Article
- PAPγ associates with PAXT nuclear exosome to control the abundance of PROMPT ncRNAs.Nature communications · 2023Article
- The Role of ncRNAs in the Immune Dysregulation of Preeclampsia.International journal of molecular sciences · 2023Review
- The polyA tail facilitates splicing of last introns with weak 3' splice sites via PABPN1.EMBO reports · 2023Article
- Mouse nuclear RNAi-defective 2 promotes splicing of weak 5' splice sites.RNA (New York, N.Y.) · 2023Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The human nuclear poly(A)-binding protein PABPN1 has been implicated in the decay of nuclear noncoding RNAs (ncRNAs). In addition, PABPN1 promotes hyperadenylation by stimulating poly(A)-polymerases (PAPα/γ), but this activity has not previously been linked to the decay of endogenous transcripts. Moreover, the mechanisms underlying target specificity have remained elusive. Here, we inactivated PAP-dependent hyperadenylation in cells by two independent mechanisms and used an RNA-seq approach to identify endogenous targets. We observed the upregulation of various ncRNAs, including snoRNA host genes, primary miRNA transcripts, and promoter upstream antisense RNAs, confirming that hyperadenylation is broadly required for the degradation of PABPN1-targets. In addition, we found that mRNAs with retained introns are susceptible to PABPN1 and PAPα/γ-mediated decay (PPD). Transcripts are targeted for degradation due to inefficient export, which is a consequence of reduced intron number or incomplete splicing. Additional investigation showed that a genetically-encoded poly(A) tail is sufficient to drive decay, suggesting that degradation occurs independently of the canonical cleavage and polyadenylation reaction. Surprisingly, treatment with transcription inhibitors uncouples polyadenylation from decay, leading to runaway hyperadenylation of nuclear decay targets. We conclude that PPD is an important mammalian nuclear RNA decay pathway for the removal of poorly spliced and nuclear-retained transcripts.
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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.