ArticlePLoS genetics2015
Mutation in MRPS34 compromises protein synthesis and causes mitochondrial dysfunction.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 47 citations in OpenAlex.
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- Mitochondrial cardiomyopathies: navigating through different clinical and management pictures between adult and paediatric forms.Frontiers in cardiovascular medicine · 2025Review
- Illuminating mitochondrial translation through mouse models.Human molecular genetics · 2024Review
- Molecular pathways in mitochondrial disorders due to a defective mitochondrial protein synthesis.Frontiers in cell and developmental biology · 2024Review
- Multi-omic profiling reveals an RNA processing rheostat that predisposes to prostate cancer.EMBO molecular medicine · 2023Article
- Mitochondrial Cardiomyopathy: Molecular Epidemiology, Diagnosis, Models, and Therapeutic Management.Cells · 2022Review
- Organization and expression of the mammalian mitochondrial genome.Nature reviews. Genetics · 2022Review
- Mitochondrial rRNA Methylation by Mettl15 Contributes to the Exercise and Learning Capability in Mice.International journal of molecular sciences · 2022Article
- A novelMolecular genetics and metabolism reports · 2022Article
- A common genetic variant of a mitochondrial RNA processing enzyme predisposes to insulin resistance.Science advances · 2021Article
- Mitochondrial mistranslation modulated by metabolic stress causes cardiovascular disease and reduced lifespan.Aging cell · 2021Article
- Mechanisms and regulation of protein synthesis in mitochondria.Nature reviews. Molecular cell biology · 2021Review
- The Diseased Mitoribosome.FEBS letters · 2021Review
- Uniparental isodisomy of chromosome 2 causing MRPL44-related multisystem mitochondrial disease.Molecular biology reports · 2021Article
- Mitochondrial Protein Translation: Emerging Roles and Clinical Significance in Disease.Frontiers in cell and developmental biology · 2021Review
- The Gene Expression Analysis of Peripheral Blood Monocytes From Psoriasis Vulgaris Patients With Different Traditional Chinese Medicine Syndromes.Frontiers in pharmacology · 2021Article
- Stress signaling and cellular proliferation reverse the effects of mitochondrial mistranslation.The EMBO journal · 2019Article
- Fidelity of translation initiation is required for coordinated respiratory complex assembly.Science advances · 2019Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The evolutionary divergence of mitochondrial ribosomes from their bacterial and cytoplasmic ancestors has resulted in reduced RNA content and the acquisition of mitochondria-specific proteins. The mitochondrial ribosomal protein of the small subunit 34 (MRPS34) is a mitochondria-specific ribosomal protein found only in chordates, whose function we investigated in mice carrying a homozygous mutation in the nuclear gene encoding this protein. The Mrps34 mutation causes a significant decrease of this protein, which we show is required for the stability of the 12S rRNA, the small ribosomal subunit and actively translating ribosomes. The synthesis of all 13 mitochondrially-encoded polypeptides is compromised in the mutant mice, resulting in reduced levels of mitochondrial proteins and complexes, which leads to decreased oxygen consumption and respiratory complex activity. The Mrps34 mutation causes tissue-specific molecular changes that result in heterogeneous pathology involving alterations in fractional shortening of the heart and pronounced liver dysfunction that is exacerbated with age. The defects in mitochondrial protein synthesis in the mutant mice are caused by destabilization of the small ribosomal subunit that affects the stability of the mitochondrial ribosome with age.
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