ArticleTranslation (Austin, Tex.)2013
Yeast telomere maintenance is globally controlled by programmed ribosomal frameshifting and the nonsense-mediated mRNA decay pathway.
Article in Translation (Austin, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Set1 regulates telomere function via H3K4 methylation-dependent and -independent pathways and calibrates the abundance of telomere maintenance factors.Molecular biology of the cell · 2023Article
- A tRNA-mimic Strategy to Explore the Role of G34 of tRNAInternational journal of molecular sciences · 2019Article
- Translational recoding signals: Expanding the synthetic biology toolbox.The Journal of biological chemistry · 2019Review
- Octa-repeat domain of the mammalian prion protein mRNA forms stable A-helical hairpin structure rather than G-quadruplexes.Scientific reports · 2019Article
- Accounting for Programmed Ribosomal Frameshifting in the Computation of Codon Usage Bias Indices.G3 (Bethesda, Md.) · 2018Article
- Small synthetic molecule-stabilized RNA pseudoknot as an activator for -1 ribosomal frameshifting.Nucleic acids research · 2018Article
- NOVA1 regulates hTERT splicing and cell growth in non-small cell lung cancer.Nature communications · 2018Article
- Overlapping open reading frames strongly reduce human and yeast STN1 gene expression and affect telomere function.PLoS genetics · 2018Article
- Translation Elongation and Recoding in Eukaryotes.Cold Spring Harbor perspectives in biology · 2018Review
- A Ribosomopathy Reveals Decoding Defective Ribosomes Driving Human Dysmorphism.American journal of human genetics · 2017Article
- Control of gene expression through the nonsense-mediated RNA decay pathway.Cell & bioscience · 2017Review
- Ribosomal frameshifting and transcriptional slippage: From genetic steganography and cryptography to adventitious use.Nucleic acids research · 2016Review
- Review
- Reprogramming the genetic code: The emerging role of ribosomal frameshifting in regulating cellular gene expression.BioEssays : news and reviews in molecular, cellular and developmental biology · 2016Review
- New Perspectives on DNA and RNA Triplexes As Effectors of Biological Activity.PLoS genetics · 2015Review
- Nonsense-mediated RNA decay--a switch and dial for regulating gene expression.BioEssays : news and reviews in molecular, cellular and developmental biology · 2015Article
- Changed in translation: mRNA recoding by -1 programmed ribosomal frameshifting.Trends in biochemical sciences · 2015Review
- The highly conserved codon following the slippery sequence supports -1 frameshift efficiency at the HIV-1 frameshift site.PloS one · 2015Article
- Ribosomes in the balance: structural equilibrium ensures translational fidelity and proper gene expression.Nucleic acids research · 2014Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We have previously shown that ~10% of all eukaryotic mRNAs contain potential programmed -1 ribosomal frameshifting (-1 PRF) signals and that some function as mRNA destabilizing elements through the Nonsense-Mediated mRNA Decay (NMD) pathway by directing translating ribosomes to premature termination codons. Here, the connection between -1 PRF, NMD and telomere end maintenance are explored. Functional -1 PRF signals were identified in the mRNAs encoding two components of yeast telomerase, EST1 and EST2, and in mRNAs encoding proteins involved in recruiting telomerase to chromosome ends, STN1 and CDC13. All of these elements responded to mutants and drugs previously known to stimulate or inhibit -1 PRF, further supporting the hypothesis that they promote -1 PRF through the canonical mechanism. All affected the steady-state abundance of a reporter mRNA and the wide range of -1 PRF efficiencies promoted by these elements enabled the determination of an inverse logarithmic relationship between -1 PRF efficiency and mRNA accumulation. Steady-state abundances of the endogenous EST1, EST2, STN1 and CDC13 mRNAs were similarly inversely proportional to changes in -1 PRF efficiency promoted by mutants and drugs, supporting the hypothesis that expression of these genes is post-transcriptionally controlled by -1 PRF under native conditions. Overexpression of EST2 by ablation of -1 PRF signals or inhibition of NMD promoted formation of shorter telomeres and accumulation of large budded cells at the G2/M boundary. A model is presented describing how limitation and maintenance of correct stoichiometries of telomerase components by -1 PRF is used to maintain yeast telomere length.
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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.