ArticleNature communications2022
Human mtRF1 terminates COX1 translation and its ablation induces mitochondrial ribosome-associated quality control.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- RMND1 dysfunction causes OXPHOS deficiency and alters mitoribosomal protein homeostasis in vivo.EMBO molecular medicine · 2026Article
- Mitochondrial DNA homeostasis: A novel therapeutic target for neurodegenerative diseases.Neural regeneration research · 2026Article
- Mitochondrial translation termination, recycling, reinitiation, and rescue for in-frame and out-of-frame contexts.Nature communications · 2026Article
- Mechanisms and disease relevance of mitochondrial translation in humans.Nature reviews. Molecular cell biology · 2026Review
- Mitochondrial translational control in cardiovascular diseases: from mechanisms to therapies.Redox biology · 2026Review
- Pleiotropic regulation of mitochondrial translational factors in governing proliferation, apoptosis and metastasis during cancer progression.World journal of clinical oncology · 2026Review
- Emerging mechanisms of human mitochondrial translation regulation.Trends in biochemical sciences · 2025Review
- Coupling of ribosome biogenesis and translation initiation in human mitochondria.Nature communications · 2025Article
- Organellar quality control crosstalk in aging-related disease: Innovation to pave the way.Aging cell · 2025Review
- Unraveling the roles and mechanisms of mitochondrial translation in normal and malignant hematopoiesis.Journal of hematology & oncology · 2024Review
- The human mitochondrial translation factor TACO1 alleviates mitoribosome stalling at polyproline stretches.Nucleic acids research · 2024Article
- The human mitochondrial mRNA structurome reveals mechanisms of gene expression.Science (New York, N.Y.) · 2024Article
- Illuminating mitochondrial translation through mouse models.Human molecular genetics · 2024Review
- Decoding the Enigma: Translation Termination in Human Mitochondria.Human molecular genetics · 2024Review
- Molecular pathways in mitochondrial disorders due to a defective mitochondrial protein synthesis.Frontiers in cell and developmental biology · 2024Review
- Structural insights into the role of GTPBP10 in the RNA maturation of the mitoribosome.Nature communications · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Translation termination requires release factors that read a STOP codon in the decoding center and subsequently facilitate the hydrolysis of the nascent peptide chain from the peptidyl tRNA within the ribosome. In human mitochondria eleven open reading frames terminate in the standard UAA or UAG STOP codon, which can be recognized by mtRF1a, the proposed major mitochondrial release factor. However, two transcripts encoding for COX1 and ND6 terminate in the non-conventional AGA or AGG codon, respectively. How translation termination is achieved in these two cases is not known. We address this long-standing open question by showing that the non-canonical release factor mtRF1 is a specialized release factor that triggers COX1 translation termination, while mtRF1a terminates the majority of other mitochondrial translation events including the non-canonical ND6. Loss of mtRF1 leads to isolated COX deficiency and activates the mitochondrial ribosome-associated quality control accompanied by the degradation of COX1 mRNA to prevent an overload of the ribosome rescue system. Taken together, these results establish the role of mtRF1 in mitochondrial translation, which had been a mystery for decades, and lead to a comprehensive picture of translation termination in human mitochondria.
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