ArticlePloS one2014
NOA1, a novel ClpXP substrate, takes an unexpected nuclear detour prior to mitochondrial import.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Molecular mechanisms of mitochondrial AAA+ proteases.The Journal of biological chemistry · 2026Review
- Recent advances in the design of small molecules targeting human ClpP.Future medicinal chemistry · 2025Review
- WTAP regulates Mitochondrial damage and Lipid oxidation in HCC by NOA1 mediated m6A modification.Journal of Cancer · 2025Article
- Massive detection of cryptic recessive genetic defects in dairy cattle mining millions of life histories.Genome biology · 2024Article
- Review
- Mitochondrial Genetic Background May Impact Statins Side Effects and Atherosclerosis Development in Familial Hypercholesterolemia.International journal of molecular sciences · 2022Article
- Proteomic analysis of the regulatory networks of ClpX in a model cyanobacteriumFrontiers in plant science · 2022Article
- Role of GTPases in Driving Mitoribosome Assembly.Trends in cell biology · 2021Review
- Imipridone Anticancer Compounds Ectopically Activate the ClpP Protease and Represent a New Scaffold for Antibiotic Development.Genetics · 2020Article
- Mitochondrial ClpX activates an essential biosynthetic enzyme through partial unfolding.eLife · 2020Article
- The AAA ATPase Afg1 preserves mitochondrial fidelity and cellular health by maintaining mitochondrial matrix proteostasis.Journal of cell science · 2018Article
- Review
- Drosophila protease ClpXP specifically degrades DmLRPPRC1 controlling mitochondrial mRNA and translation.Scientific reports · 2017Article
- Recent Insights into the Role of Unfolded Protein Response in ER Stress in Health and Disease.Frontiers in cell and developmental biology · 2017Review
- Mitochondrial Quality Control Proteases in Neuronal Welfare.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2016Review
- Site specific replacements of a single loop nucleoside with a dibenzyl linker may switch the activity of TBA from anticoagulant to antiproliferative.Nucleic acids research · 2015Article
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mitochondrial matrix GTPase NOA1 is a nuclear encoded protein, essential for mitochondrial protein synthesis, oxidative phosphorylation and ATP production. Here, we demonstrate that newly translated NOA1 protein is imported into the nucleus, where it localizes to the nucleolus and interacts with UBF1 before nuclear export and import into mitochondria. Mutation of the nuclear localization signal (NLS) prevented both nuclear and mitochondrial import while deletion of the N-terminal mitochondrial targeting sequence (MTS) or the C-terminal RNA binding domain of NOA1 impaired mitochondrial import. Absence of the MTS resulted in accumulation of NOA1 in the nucleus and increased caspase-dependent apoptosis. We also found that export of NOA1 from the nucleus requires a leptomycin-B sensitive, Crm1-dependent nuclear export signal (NES). Finally, we show that NOA1 is a new substrate of the mitochondrial matrix protease complex ClpXP. Our results uncovered an unexpected, mandatory detour of NOA1 through the nucleolus before uptake into mitochondria. We propose that nucleo-mitochondrial translocation of proteins is more widespread than previously anticipated providing additional means to control protein bioavailability as well as cellular communication between both compartments.
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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.