ArticleProceedings of the National Academy of Sciences of the United States of America2020
Metabolic stress promotes stop-codon readthrough and phenotypic heterogeneity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
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- Serine mistranslation induces the integrated stress response through the P stalk.The Journal of biological chemistry · 2025Article
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- Suppression of amber stop codons impairs pathogenicity in Salmonella.FEBS letters · 2025Article
- The impact of phenotypic heterogeneity on fungal pathogenicity and drug resistance.FEMS microbiology reviews · 2025Review
- Environment modulates protein heterogeneity through transcriptional and translational stop codon readthrough.Nature communications · 2024Article
- Fluorescent reporters give new insights into antibiotics-induced nonsense and frameshift mistranslation.Scientific reports · 2024Article
- Misincorporations of amino acids in p53 in human cells at artificially constructed termination codons in the presence of the aminoglycoside Gentamicin.Frontiers in genetics · 2024Article
- Polyaminated, acetylated and stop codon readthrough of recombinant Francisella tularensis universal stress protein in Escherichia coli.PloS one · 2024Article
- Genome-wide screening reveals metabolic regulation of stop-codon readthrough by cyclic AMP.Nucleic acids research · 2023Article
- Evolution of termination codons of proteins and the TAG-TGA paradox.Scientific reports · 2023Article
- Evaluation of Novel Enhancer Compounds in Gentamicin-Mediated Readthrough of Nonsense Mutations in Rett Syndrome.International journal of molecular sciences · 2023Article
- Mistranslation of the genetic code by a new family of bacterial transfer RNAs.The Journal of biological chemistry · 2023Article
- Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Accurate protein synthesis is a tightly controlled biological process with multiple quality control steps safeguarded by aminoacyl-transfer RNA (tRNA) synthetases and the ribosome. Reduced translational accuracy leads to various physiological changes in both prokaryotes and eukaryotes. Termination of translation is signaled by stop codons and catalyzed by release factors. Occasionally, stop codons can be suppressed by near-cognate aminoacyl-tRNAs, resulting in protein variants with extended C termini. We have recently shown that stop-codon readthrough is heterogeneous among single bacterial cells. However, little is known about how environmental factors affect the level and heterogeneity of stop-codon readthrough. In this study, we have combined dual-fluorescence reporters, mass spectrometry, mathematical modeling, and single-cell approaches to demonstrate that a metabolic stress caused by excess carbon substantially increases both the level and heterogeneity of stop-codon readthrough. Excess carbon leads to accumulation of acid metabolites, which lower the pH and the activity of release factors to promote readthrough. Furthermore, our time-lapse microscopy experiments show that single cells with high readthrough levels are more adapted to severe acid stress conditions and are more sensitive to an aminoglycoside antibiotic. Our work thus reveals a metabolic stress that promotes translational heterogeneity and phenotypic diversity.
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