{"title":"衰老相关的翻译下降是转录失调的结果。","authors":"Sebastian Pechmann","doi":"10.1098/rsif.2025.0323","DOIUrl":null,"url":null,"abstract":"<p><p>The ageing-related decline of translational fidelity disrupts cellular protein homeostasis, thus contributing to the onset of cancer and neurodegeneration. However, it remains unclear what alters speed and accuracy of translation at advanced age. Here, I show that the shift in translation kinetics upon ageing is systematic and a direct consequence of transcription deregulation. Computational modelling of ageing yeast and worm Riboseq data demonstrates that the loss of translational fidelity is independent of codon identity, tRNA abundances or the specificities of anticodon-codon interactions at the ribosome. Instead, large-scale transcriptional changes during ageing perturb the codon usage of the transcriptome, which at the systems level induces a dramatic remodelling and increase in ribosome collisions and stalling. Ribosome collisions in turn reduce control over translation elongation and effect an assimilation of codon translation rates. The presented results thus explain the ageing-related decline of translational fidelity, and provide important insights towards a systems-level understanding of ageing-related human diseases linked to mistranslation and protein homeostasis failure that are especially prevalent in the brain.</p>","PeriodicalId":17488,"journal":{"name":"Journal of The Royal Society Interface","volume":"22 230","pages":"20250323"},"PeriodicalIF":3.5000,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12457020/pdf/","citationCount":"0","resultStr":"{\"title\":\"Ageing-related decline of translation as a consequence of transcription dysregulation.\",\"authors\":\"Sebastian Pechmann\",\"doi\":\"10.1098/rsif.2025.0323\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The ageing-related decline of translational fidelity disrupts cellular protein homeostasis, thus contributing to the onset of cancer and neurodegeneration. However, it remains unclear what alters speed and accuracy of translation at advanced age. Here, I show that the shift in translation kinetics upon ageing is systematic and a direct consequence of transcription deregulation. Computational modelling of ageing yeast and worm Riboseq data demonstrates that the loss of translational fidelity is independent of codon identity, tRNA abundances or the specificities of anticodon-codon interactions at the ribosome. Instead, large-scale transcriptional changes during ageing perturb the codon usage of the transcriptome, which at the systems level induces a dramatic remodelling and increase in ribosome collisions and stalling. Ribosome collisions in turn reduce control over translation elongation and effect an assimilation of codon translation rates. The presented results thus explain the ageing-related decline of translational fidelity, and provide important insights towards a systems-level understanding of ageing-related human diseases linked to mistranslation and protein homeostasis failure that are especially prevalent in the brain.</p>\",\"PeriodicalId\":17488,\"journal\":{\"name\":\"Journal of The Royal Society Interface\",\"volume\":\"22 230\",\"pages\":\"20250323\"},\"PeriodicalIF\":3.5000,\"publicationDate\":\"2025-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12457020/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of The Royal Society Interface\",\"FirstCategoryId\":\"103\",\"ListUrlMain\":\"https://doi.org/10.1098/rsif.2025.0323\",\"RegionNum\":2,\"RegionCategory\":\"综合性期刊\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/9/24 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"MULTIDISCIPLINARY SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of The Royal Society Interface","FirstCategoryId":"103","ListUrlMain":"https://doi.org/10.1098/rsif.2025.0323","RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/9/24 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"MULTIDISCIPLINARY SCIENCES","Score":null,"Total":0}
Ageing-related decline of translation as a consequence of transcription dysregulation.
The ageing-related decline of translational fidelity disrupts cellular protein homeostasis, thus contributing to the onset of cancer and neurodegeneration. However, it remains unclear what alters speed and accuracy of translation at advanced age. Here, I show that the shift in translation kinetics upon ageing is systematic and a direct consequence of transcription deregulation. Computational modelling of ageing yeast and worm Riboseq data demonstrates that the loss of translational fidelity is independent of codon identity, tRNA abundances or the specificities of anticodon-codon interactions at the ribosome. Instead, large-scale transcriptional changes during ageing perturb the codon usage of the transcriptome, which at the systems level induces a dramatic remodelling and increase in ribosome collisions and stalling. Ribosome collisions in turn reduce control over translation elongation and effect an assimilation of codon translation rates. The presented results thus explain the ageing-related decline of translational fidelity, and provide important insights towards a systems-level understanding of ageing-related human diseases linked to mistranslation and protein homeostasis failure that are especially prevalent in the brain.
期刊介绍:
J. R. Soc. Interface welcomes articles of high quality research at the interface of the physical and life sciences. It provides a high-quality forum to publish rapidly and interact across this boundary in two main ways: J. R. Soc. Interface publishes research applying chemistry, engineering, materials science, mathematics and physics to the biological and medical sciences; it also highlights discoveries in the life sciences of relevance to the physical sciences. Both sides of the interface are considered equally and it is one of the only journals to cover this exciting new territory. J. R. Soc. Interface welcomes contributions on a diverse range of topics, including but not limited to; biocomplexity, bioengineering, bioinformatics, biomaterials, biomechanics, bionanoscience, biophysics, chemical biology, computer science (as applied to the life sciences), medical physics, synthetic biology, systems biology, theoretical biology and tissue engineering.