ArticleCommunications biology2021
Random errors in protein synthesis activate an age-dependent program of muscle atrophy in mice.
Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Error-prone translation as a driver of proteostasis collapse and neurodegeneration.Neural regeneration research · 2026Article
- Translational error in mice increases with ageing in an organ-dependent manner.Nature communications · 2025Article
- Appetitively motivated tasks in the IntelliCage reveal a higher motivational cost of spatial learning in male than female mice.Frontiers in behavioral neuroscience · 2024Article
- Article
- Ribosomal Protein uS5 and Friends: Protein-Protein Interactions Involved in Ribosome Assembly and Beyond.Biomolecules · 2023Review
- Premature aging in mice with error-prone protein synthesis.Science advances · 2022Article
- Silencing of the ER and Integrative Stress Responses in the Liver of Mice with Error-Prone Translation.Cells · 2021Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Random errors in protein synthesis are prevalent and ubiquitous, yet their effect on organismal health has remained enigmatic for over five decades. Here, we studied whether mice carrying the ribosomal ambiguity (ram) mutation Rps2-A226Y, recently shown to increase the inborn error rate of mammalian translation, if at all viable, present any specific, possibly aging-related, phenotype. We introduced Rps2-A226Y using a Cre/loxP strategy. Resulting transgenic mice were mosaic and showed a muscle-related phenotype with reduced grip strength. Analysis of gene expression in skeletal muscle using RNA-Seq revealed transcriptomic changes occurring in an age-dependent manner, involving an interplay of PGC1α, FOXO3, mTOR, and glucocorticoids as key signaling pathways, and finally resulting in activation of a muscle atrophy program. Our results highlight the relevance of translation accuracy, and show how disturbances thereof may contribute to age-related pathologies.
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Registered trials
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