ArticleCell2016
The DEAD-Box Protein Dhh1p Couples mRNA Decay and Translation by Monitoring Codon Optimality.
Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers, 1 of them a synthesis that pooled it.
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Who cites it
170 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Synonymous but Not Silent: The Codon Usage Code for Gene Expression and Protein Folding.Annual review of biochemistry · 2021Pooled it
- Global Regulatory Functions of the Human CCR4-NOT Complex in mRNA Deadenylation and Decay.bioRxiv : the preprint server for biology · 2026Article
- Codon optimality predicts mRNA half-life but does not transfer to lncRNAs.Molecular genetics and genomics : MGG · 2026Article
- Beyond codon optimality: codon pairs regulate mRNA stability dependent on translation.bioRxiv : the preprint server for biology · 2026Article
- Deadenylation and decapping factors cooperatively stimulate biochemical activities of DEAD-box ATPase Dhh1.Nucleic acids research · 2026Article
- Nascent chain folding status modulates ribosome dynamics and mRNA stability through the ribosome-associated chaperone Zuo1.Molecular cell · 2026Article
- Deadenylation and Decapping Factors Cooperatively Stimulate Biochemical Activities of DEAD-Box ATPase Dhh1.bioRxiv : the preprint server for biology · 2026Article
- predNMD: prediction of nonsense-mediated mRNA decay for improved clinical variant pathogenicity classification.bioRxiv : the preprint server for biology · 2026Article
- Transcripts enriched in codons that trigger P-site tRNA-mediated mRNA decay possess stable mRNA.FEBS open bio · 2026Article
- Degradation factor 1, Def1, regulates mRNA translation and decay through Ccr4-Not-dependent ubiquitylation of the ribosome.RNA (New York, N.Y.) · 2026Article
- Degradation factor 1, Def1, regulates mRNA translation and decay through Ccr4-Not-dependent ubiquitylation of the ribosome.bioRxiv : the preprint server for biology · 2025Article
- Article
- Functional synonymous mutations and their evolutionary consequences.Nature reviews. Genetics · 2025Review
- Codon Composition in Human Oocytes Reveals Age-Associated Defects in mRNA Decay.International journal of molecular sciences · 2025Article
- DDX6 interacts with DDX3X to repress translation in microRNA-mediated silencing.Nucleic acids research · 2025Article
- Decapping activators Edc3 and Scd6 act redundantly with Dhh1 in post-transcriptional repression of starvation-induced pathways.bioRxiv : the preprint server for biology · 2025Article
- Cytoplasmic mRNA decay and quality control machineries in eukaryotes.Nature reviews. Genetics · 2025Review
- Roles of P-body factors inbioRxiv : the preprint server for biology · 2025Article
- Decoding subcellular RNA localization one molecule at a time.Genome biology · 2025Review
- Roles of P-body factors in Candida albicans filamentation and stress response.PLoS genetics · 2025Article
110 more citing papers are in PubMed but not listed here.
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6 authors.
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Abstract
A major determinant of mRNA half-life is the codon-dependent rate of translational elongation. How the processes of translational elongation and mRNA decay communicate is unclear. Here, we establish that the DEAD-box protein Dhh1p is a sensor of codon optimality that targets an mRNA for decay. First, we find mRNAs whose translation elongation rate is slowed by inclusion of non-optimal codons are specifically degraded in a Dhh1p-dependent manner. Biochemical experiments show Dhh1p is preferentially associated with mRNAs with suboptimal codon choice. We find these effects on mRNA decay are sensitive to the number of slow-moving ribosomes on an mRNA. Moreover, we find Dhh1p overexpression leads to the accumulation of ribosomes specifically on mRNAs (and even codons) of low codon optimality. Lastly, Dhh1p physically interacts with ribosomes in vivo. Together, these data argue that Dhh1p is a sensor for ribosome speed, targeting an mRNA for repression and subsequent decay.
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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.