ArticlePLoS genetics2014
Ribosome rescue and translation termination at non-standard stop codons by ICT1 in mammalian mitochondria.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 76 citations in OpenAlex.
- 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
- Pleiotropic regulation of mitochondrial translational factors in governing proliferation, apoptosis and metastasis during cancer progression.World journal of clinical oncology · 2026Review
- Knockout of the mitoribosome rescue factors Ict1 or Mtrfr is viable in zebrafish but not mice: compensatory mechanisms underlying each factor's loss.FEBS open bio · 2025Article
- Emerging mechanisms of human mitochondrial translation regulation.Trends in biochemical sciences · 2025Review
- Unraveling the roles and mechanisms of mitochondrial translation in normal and malignant hematopoiesis.Journal of hematology & oncology · 2024Review
- 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
- Cytosolic protein translation regulates cell asymmetry and function in early TCR activation of human CD8Frontiers in immunology · 2024Article
- Mutation of the PEBP-like domain of the mitoribosomal MrpL35/mL38 protein results in production of nascent chains with impaired capacity to assemble into OXPHOS complexes.Molecular biology of the cell · 2023Article
- Translation in Mitochondrial Ribosomes.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Nonstop mRNAs generate a ground state of mitochondrial gene expression noise.Science advances · 2022Article
- Organization and expression of the mammalian mitochondrial genome.Nature reviews. Genetics · 2022Review
- Balanced mitochondrial and cytosolic translatomes underlie the biogenesis of human respiratory complexes.Genome biology · 2022Article
- Mammalian HEMK1 methylates glutamine residue of the GGQ motif of mitochondrial release factors.Scientific reports · 2022Article
- Maintaining mitochondrial ribosome function: The role of ribosome rescue and recycling factors.RNA biology · 2022Review
- Diversity and Similarity of Termination and Ribosome Rescue in Bacterial, Mitochondrial, and Cytoplasmic Translation.Biochemistry. Biokhimiia · 2021Review
- Mechanisms and regulation of protein synthesis in mitochondria.Nature reviews. Molecular cell biology · 2021Review
- A stalled-ribosome rescue factor Pth3 is required for mitochondrial translation against antibiotics in Saccharomyces cerevisiae.Communications biology · 2021Article
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4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Release factors (RFs) govern the termination phase of protein synthesis. Human mitochondria harbor four different members of the class 1 RF family: RF1Lmt/mtRF1a, RF1mt, C12orf65 and ICT1. The homolog of the essential ICT1 factor is widely distributed in bacteria and organelles and has the peculiar feature in human mitochondria to be part of the ribosome as a ribosomal protein of the large subunit. The factor has been suggested to rescue stalled ribosomes in a codon-independent manner. The mechanism of action of this factor was obscure and is addressed here. Using a homologous mitochondria system of purified components, we demonstrate that the integrated ICT1 has no rescue activity. Rather, purified ICT1 binds stoichiometrically to mitochondrial ribosomes in addition to the integrated copy and functions as a general rescue factor, i.e. it releases the polypeptide from the peptidyl tRNA from ribosomes stalled at the end or in the middle of an mRNA or even from non-programmed ribosomes. The data suggest that the unusual termination at a sense codon (AGA/G) of the oxidative-phosphorylation enzymes CO1 and ND6 is also performed by ICT1 challenging a previous model, according to which RF1Lmt/mtRF1a is responsible for the translation termination at non-standard stop codons. We also demonstrate by mutational analyses that the unique insertion sequence present in the N-terminal domain of ICT1 is essential for peptide release rather than for ribosome binding. The function of RF1mt, another member of the class1 RFs in mammalian mitochondria, was also examined and is discussed.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.