ArticleiScience2021
Protease OMA1 modulates mitochondrial bioenergetics and ultrastructure through dynamic association with MICOS complex.
Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
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Who cites it
29 citing papers in PubMed, 40 citations in OpenAlex.
- 3-Hydroxypropanoic acid contributing to pollen abortion in ogura cytoplasmic male sterility of Brassica napus.BMC plant biology · 2026Article
- FAM162A Is a Key Regulator of Mitochondrial Structure, Dynamics, and Bioenergetics, Driving Cellular Protection and Longevity.Aging cell · 2026Article
- The MICOS Complex Regulates Mitochondrial Structure and Oxidative Stress During Age-Dependent Structural Deficits in the Kidney.Aging cell · 2026Article
- Cristae: bridging bioenergetic hubs and compartmental barriers in mitochondrial homeostasis.Cell death & disease · 2026Review
- Atypical Phenotypes of Mitochondrial Cristae Architecture in Selected Human Aging Striated Muscles-Transmission Electron Microscope Studies.Life (Basel, Switzerland) · 2026Article
- The MICOS Complex Regulates Mitochondrial Structure and Oxidative Stress During Age-Dependent Structural Deficits in the Kidney.bioRxiv : the preprint server for biology · 2026Article
- Stress adaptation of mitochondrial protein import by OMA1-mediated degradation of DNAJC15.Nature structural & molecular biology · 2026Article
- Molecular machineries shaping the mitochondrial inner membrane.Nature reviews. Molecular cell biology · 2025Review
- HThe Journal of biological chemistry · 2025Article
- Mitochondrial dysfunction in Alzheimer's disease: Guiding the path to targeted therapies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Compositionally unique mitochondria in filopodia support cellular migration.Current biology : CB · 2025Article
- Mitochondrial membrane synthesis, remodelling and cellular trafficking.Journal of inherited metabolic disease · 2025Review
- SLP2 and MIC13 synergistically coordinate MICOS assembly and crista junction formation.iScience · 2024Article
- Differentiation activates mitochondrial OPA1 processing in myoblast cell lines.Mitochondrion · 2024Article
- Opa1 processing is dispensable in mouse development but is protective in mitochondrial cardiomyopathy.Science advances · 2024Article
- Compositionally unique mitochondria in filopodia support cellular migration.bioRxiv : the preprint server for biology · 2024Article
- OMA1 protease eliminates arrested protein import intermediates upon mitochondrial depolarization.The Journal of cell biology · 2024Article
- OMA1-Mediated Mitochondrial Dynamics Balance Organellar Homeostasis Upstream of Cellular Stress Responses.International journal of molecular sciences · 2024Review
- Vitamin D ameliorates age-induced nonalcoholic fatty liver disease by increasing the mitochondrial contact site and cristae organizing system (MICOS) 60 level.Experimental & molecular medicine · 2024Article
- An OMA1 redox site controls mitochondrial homeostasis, sarcoma growth, and immunogenicity.Life science alliance · 2023Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Remodeling of mitochondrial ultrastructure is a process that is critical for organelle physiology and apoptosis. Although the key players in this process-mitochondrial contact site and cristae junction organizing system (MICOS) and Optic Atrophy 1 (OPA1)-have been characterized, the mechanisms behind its regulation remain incompletely defined. Here, we found that in addition to its role in mitochondrial division, metallopeptidase OMA1 is required for the maintenance of intermembrane connectivity through dynamic association with MICOS. This association is independent of OPA1, mediated via the MICOS subunit MIC60, and is important for stability of MICOS and the intermembrane contacts. The OMA1-MICOS relay is required for optimal bioenergetic output and apoptosis. Loss of OMA1 affects these activities; remarkably it can be alleviated by MICOS-emulating intermembrane bridge. Thus, OMA1-dependent ultrastructure support is required for mitochondrial architecture and bioenergetics under basal and stress conditions, suggesting a previously unrecognized role for OMA1 in mitochondrial physiology.
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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.