ArticleScience advances2022
Nonstop mRNAs generate a ground state of mitochondrial gene expression noise.
Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- 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
- Towards a mitogenomic phylogeny of mud dragons (Kinorhyncha): two new mitogenomes from the Pycnophyidae family.Scientific reports · 2026Article
- 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
- The mitochondrial methylation potential gates mitoribosome assembly.Nature communications · 2025Article
- Evaluating the feasibility of gene replacement strategies to treat MTRFR deficiency.Disease models & mechanisms · 2025Article
- Mitochondrial protein synthesis quality control.Human molecular genetics · 2024Review
- A kinetic dichotomy between mitochondrial and nuclear gene expression processes.Molecular cell · 2024Article
- A kinetic dichotomy between mitochondrial and nuclear gene expression drives OXPHOS biogenesis.bioRxiv : the preprint server for biology · 2023Article
- A small protein coded within the mitochondrial canonical gene nd4 regulates mitochondrial bioenergetics.BMC biology · 2023Article
- Mitochondrial polymorphism m.3017C>T of SHLP6 relates to heterothermy.Frontiers in physiology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
A stop codon within the mRNA facilitates coordinated termination of protein synthesis, releasing the nascent polypeptide from the ribosome. This essential step in gene expression is impeded with transcripts lacking a stop codon, generating nonstop ribosome complexes. Here, we use deep sequencing to investigate sources of nonstop mRNAs generated from the human mitochondrial genome. We identify diverse types of nonstop mRNAs on mitochondrial ribosomes that are resistant to translation termination by canonical release factors. Failure to resolve these aberrations by the mitochondrial release factor in rescue (MTRFR) imparts a negative regulatory effect on protein synthesis that is associated with human disease. Our findings reveal a source of underlying noise in mitochondrial gene expression and the importance of responsive ribosome quality control mechanisms for cell fitness and human health.
Identifiers
What OpenQuestion holds
Registered trials
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.