Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (434 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The sequential set of three nucleotides in transfer rna that interacts with its complement in messenger rna, the codon, during translation in the ribosome.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Anticodons.
Where it fits in the MeSH classification
- Broader topics
- RNA, Transfer; Genetic Code
Related concepts
- Transfer Rna
- Messenger Rna
- Codon
Research landscape
PubMed indexes 2,134 records tagged with the MeSH heading “Anticodon” (counts retrieved 2026-10-29). 240 of them (11.2%) were published from 2020 onward, and the busiest period so far is through 1999 with 1,080 records.
Reviews account for 204 records (9.6%) and meta-analyses for 0. Randomized controlled trials number 0 (0.0%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,080 |
| 2000-2009 | 439 |
| 2010-2019 | 375 |
| 2020 onward | 240 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 204 | 9.6% |
| Meta-analyses | 0 | 0.0% |
| Randomized controlled trials | 0 | 0.0% |
Method: PubMed query "Anticodon"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in genetics and genomics
Genetic findings vary widely in strength. A variant linked to a condition in one study may not replicate in other ancestries, and most common variants have small effects that are meaningful only in aggregate. Studies of rare, high-impact variants can support strong causal claims about a gene, while association studies describe statistical links that need functional and independent replication. Check the sample size, the ancestry of participants, whether results were replicated, and whether a laboratory or clinical outcome was actually measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Loss of a conserved tRNA anticodon modification perturbs cellular signaling | 2013 | Research article Design not recorded in structured metadata | 193 | cc by PMID 23935536 · DOI · PMC3731203 |
| Genome recoding by tRNA modifications | 2016 | Review article Design not recorded in structured metadata | 86 | cc by PMID 27974624 · DOI · PMC5204126 |
| Selective gene expression maintains human tRNA anticodon pools during differentiation | 2024 | Research article Design not recorded in structured metadata | 82 | cc by PMID 38191669 · DOI · PMC10791582 |
Loss of a conserved tRNA anticodon modification perturbs cellular signaling [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Transfer RNA (tRNA) modifications enhance the efficiency, specificity and fidelity of translation in all organisms.
- Closing excerpt
- Thus, loss of mcm(5)s(2)U causes global effects on gene expression due to perturbation of cellular signaling.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (148 words)
Transfer RNA (tRNA) modifications enhance the efficiency, specificity and fidelity of translation in all organisms. The anticodon modification mcm(5)s(2)U(34) is required for normal growth and stress resistance in yeast; mutants lacking this modification have numerous phenotypes. Mutations in the homologous human genes are linked to neurological disease. The yeast phenotypes can be ameliorated by overexpression of specific tRNAs, suggesting that the modifications are necessary for efficient translation of specific codons. We determined the in vivo ribosome distributions at single codon resolution in yeast strains lacking mcm(5)s(2)U. We found accumulations at AAA, CAA, and GAA codons, suggesting that translation is slow when these codons are in the ribosomal A site, but these changes appeared too small to affect protein output. Instead, we observed activation of the GCN4-mediated stress response by a non-canonical pathway. Thus, loss of mcm(5)s(2)U causes global effects on gene expression due to perturbation of cellular signaling.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 23935536 · DOI · PMC3731203
Genome recoding by tRNA modifications [2]
Abstract reading summary — source excerpts
- Opening excerpt
- RNA modifications are emerging as an additional regulatory layer on top of the primary RNA sequence.
- Closing excerpt
- We discuss the functional relevance of these modifications in protein translation and their emerging role in eukaryotic genome recoding during cellular adaptation and disease.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (129 words)
RNA modifications are emerging as an additional regulatory layer on top of the primary RNA sequence. These modifications are particularly enriched in tRNAs where they can regulate not only global protein translation, but also protein translation at the codon level. Modifications located in or in the vicinity of tRNA anticodons are highly conserved in eukaryotes and have been identified as potential regulators of mRNA decoding. Recent studies have provided novel insights into how these modifications orchestrate the speed and fidelity of translation to ensure proper protein homeostasis. This review highlights the prominent modifications in the tRNA anticodon loop: queuosine, inosine, 5-methoxycarbonylmethyl-2-thiouridine, wybutosine, threonyl-carbamoyl-adenosine and 5-methylcytosine. We discuss the functional relevance of these modifications in protein translation and their emerging role in eukaryotic genome recoding during cellular adaptation and disease.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 27974624 · DOI · PMC5204126
Selective gene expression maintains human tRNA anticodon pools during differentiation [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Transfer RNAs are essential for translating genetic information into proteins.
- Closing excerpt
- Our data explain how tRNA anticodon pools are buffered to maintain decoding speed across cell types and reveal that mTORC1 drives selective tRNA expression during differentiation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (157 words)
Transfer RNAs are essential for translating genetic information into proteins. The human genome contains hundreds of predicted tRNA genes, many in multiple copies. How their expression is regulated to control tRNA repertoires is unknown. Here we combined quantitative tRNA profiling and chromatin immunoprecipitation with sequencing to measure tRNA expression following the differentiation of human induced pluripotent stem cells into neuronal and cardiac cells. We find that tRNA transcript levels vary substantially, whereas tRNA anticodon pools, which govern decoding rates, are more stable among cell types. Mechanistically, RNA polymerase III transcribes a wide range of tRNA genes in human induced pluripotent stem cells but on differentiation becomes constrained to a subset we define as housekeeping tRNAs. This shift is mediated by decreased mTORC1 signalling, which activates the RNA polymerase III repressor MAF1. Our data explain how tRNA anticodon pools are buffered to maintain decoding speed across cell types and reveal that mTORC1 drives selective tRNA expression during differentiation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38191669 · DOI · PMC10791582
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Preferential codon usage in prokaryotic genes: the optimal codon-anticodon interaction energy and the selective codon usage in efficiently expressed genes [4]
- Research article tRNA's wobble decoding of the genome: 40 years of modification [5]
- Research article tRNA's modifications bring order to gene expression [6]
- Research article The transfer RNA identity problem: a search for rules [7]
- Research article A rationale for tRNA modification circuits in the anticodon loop [8]
- Research article The Importance of Being Modified: The Role of RNA Modifications in Translational Fidelity [9]
References
- Zinshteyn B, Gilbert WV. Loss of a conserved tRNA anticodon modification perturbs cellular signaling. . 2013. PMID 23935536 · DOI · PMC3731203
- Tuorto F, Lyko F. Genome recoding by tRNA modifications. . 2016. PMID 27974624 · DOI · PMC5204126
- Gao L, Behrens A, Rodschinka G, Forcelloni S, Wani S, Strasser K, et al.. Selective gene expression maintains human tRNA anticodon pools during differentiation. . 2024. PMID 38191669 · DOI · PMC10791582
- Grosjean H, Fiers W. Preferential codon usage in prokaryotic genes: the optimal codon-anticodon interaction energy and the selective codon usage in efficiently expressed genes. Gene. 1982. PMID 6751939 · DOI
- Agris PF, Vendeix FA, Graham WD. tRNA's wobble decoding of the genome: 40 years of modification. J Mol Biol. 2007. PMID 17187822 · DOI
- Gustilo EM, Vendeix FA, Agris PF. tRNA's modifications bring order to gene expression. Curr Opin Microbiol. 2008. PMID 18378185 · DOI · PMC2408636
- Saks ME, Sampson JR, Abelson JN. The transfer RNA identity problem: a search for rules. Science. 1994. PMID 7506844 · DOI
- Han L, Phizicky EM. A rationale for tRNA modification circuits in the anticodon loop. RNA. 2018. PMID 30026310 · DOI · PMC6140457
- Agris PF, Narendran A, Sarachan K, Väre VYP, Eruysal E. The Importance of Being Modified: The Role of RNA Modifications in Translational Fidelity. Enzymes. 2017. PMID 28601219 · DOI · PMC8118379
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.