ArticleThe Journal of cell biology2024
OMA1 protease eliminates arrested protein import intermediates upon mitochondrial depolarization.
Article in The Journal of cell biology, 2024. 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, 27 citations in OpenAlex.
- Cholesterol-driven mitochondrial rejuvenation by quercetin nanotherapeutics restores implant osseointegration in diabetes.Bioactive materials · 2026Article
- Clean cut to curtail respiration: OMA1 cleaves AIFM1 to tune stress-induced bioenergetics.The EMBO journal · 2026Article
- Proteolytic control of mitochondrial protein translocases.Protein science : a publication of the Protein Society · 2026Review
- Quality control of protein import into mammalian mitochondria.Protein science : a publication of the Protein Society · 2026Review
- Stress adaptation of mitochondrial protein import by OMA1-mediated degradation of DNAJC15.Nature structural & molecular biology · 2026Article
- In and out of the mitochondrial intermembrane space.Protein science : a publication of the Protein Society · 2026Review
- Function and regulation of the mitochondrial stress response.Nature structural & molecular biology · 2026Review
- A unified mechanism for mitochondrial damage sensing in PINK1-Parkin-mediated mitophagy.The EMBO journal · 2026Article
- Article
- The many faces of p97/Cdc48 in mitochondrial homeostasis.Essays in biochemistry · 2025Review
- Mitochondrial proteases and their roles in mitophagy in plants, animals, and yeast.Plant & cell physiology · 2025Review
- Tom40 functions as a channel for protein retrotranslocation in the mitochondria-associated degradation (MAD) pathway.Communications biology · 2025Article
- Mitochondria - the CEO of the cell.Journal of cell science · 2025Review
- A long-lived pool of PINK1 imparts a molecular memory of depolarization-induced activity.Science advances · 2025Article
- Mitochondrial YME1L1 governs unoccupied protein translocase channels.Nature cell biology · 2025Article
- Mitochondrial protein import stress.Nature cell biology · 2025Review
- Hypotonic Swelling Method for the Isolation of Pure Mitochondria From Primary Human Skeletal Myoblasts for Proteomic Studies.Journal of cellular and molecular medicine · 2025Article
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Most mitochondrial proteins originate from the cytosol and require transport into the organelle. Such precursor proteins must be unfolded to pass through translocation channels in mitochondrial membranes. Misfolding of transported proteins can result in their arrest and translocation failure. Arrested proteins block further import, disturbing mitochondrial functions and cellular proteostasis. Cellular responses to translocation failure have been defined in yeast. We developed the cell line-based translocase clogging model to discover molecular mechanisms that resolve failed import events in humans. The mechanism we uncover differs significantly from these described in fungi, where ATPase-driven extraction of blocked protein is directly coupled with proteasomal processing. We found human cells to rely primarily on mitochondrial factors to clear translocation channel blockage. The mitochondrial membrane depolarization triggered proteolytic cleavage of the stalled protein, which involved mitochondrial protease OMA1. The cleavage allowed releasing the protein fragment that blocked the translocase. The released fragment was further cleared in the cytosol by VCP/p97 and the proteasome.
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Registered trials
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