ArticleCommunications biology2023
TUT4/7-mediated uridylation of a coronavirus subgenomic RNAs delays viral replication.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 12 citations in OpenAlex.
- RNA terminal uridylyl transferases are druggable vulnerabilities in AML but are dispensable for normal hematopoiesis.Science advances · 2026Article
- The TENT5A-ATXN2 axis modulates germline and somatic cell survival during heat stress.Cell death & disease · 2026Article
- TENT5C extends Odf1 poly(A) tail to sustain sperm morphogenesis and fertility.Nature communications · 2026Article
- mRNA poly(A)-tail length is a battleground for coronavirus-host competition.bioRxiv : the preprint server for biology · 2025Article
- TENT5C functions as a corepressor in the ligand-bound glucocorticoid receptor and estrogen receptor α complexes.The FEBS journal · 2025Article
- Noncanonical Poly(A) Polymerase TENT4 Drives Expression of Subgenomic Hepatitis A Virus RNAs in Infected Cells.Viruses · 2025Article
- RNA Editors Sculpt the Transcriptome During Terminal Erythropoiesis.Research square · 2025Article
- Rapid and accurate demultiplexing of direct RNA nanopore sequencing data with SeqTagger.Genome research · 2025Article
- Role of the epitranscriptome in viral infections: beneficial or detrimental?Memorias do Instituto Oswaldo Cruz · 2025Review
- Dual Roles of Host Zinc Finger Proteins in Viral RNA Regulation: Decay or Stabilization.International journal of molecular sciences · 2024Review
- The Battle for Survival: The Role of RNA Non-Canonical Tails in the Virus-Host Interaction.Metabolites · 2023Review
- The regulation of antiviral innate immunity through non-mFrontiers in immunology · 2023Review
- Revealing the hidden RBP-RNA interactions with RNA modification enzyme-based strategies.Wiley interdisciplinary reviews. RNAReview
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Coronaviruses are positive-strand RNA viruses with 3' polyadenylated genomes and subgenomic transcripts. The lengths of the viral poly(A) tails change during infection by mechanisms that remain poorly understood. Here, we use a splint-ligation method to measure the poly(A) tail length and poly(A) terminal uridylation and guanylation of the mouse hepatitis virus (MHV) RNAs. Upon infection of 17-CL1 cells with MHV, a member of the Betacoronavirus genus, we observe two populations of terminally uridylated viral transcripts, one with poly(A) tails ~44 nucleotides long and the other with poly(A) tails shorter than ~22 nucleotides. The mammalian terminal uridylyl-transferase 4 (TUT4) and terminal uridylyl-transferase 7 (TUT7), referred to as TUT4/7, add non-templated uracils to the 3'-end of endogenous transcripts with poly(A) tails shorter than ~30 nucleotides to trigger transcript decay. Here we find that depletion of the host TUT4/7 results in an increased replication capacity of the MHV virus. At late stages of infection, the population of uridylated subgenomic RNAs with tails shorter than ~22 nucleotides is reduced in the absence of TUT4/7 while the viral RNA load increases. Our findings indicate that TUT4/7 uridylation marks the MHV subgenomic RNAs for decay and delays viral replication.
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Registered trials
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