ArticleCellular signalling2015
Differential submitochondrial localization of PINK1 as a molecular switch for mediating distinct mitochondrial signaling pathways.
Article in Cellular signalling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- Inter-Organelle Membrane Contact Sites as Physiological Regulatory Hubs in the Brain: From Neurons to Glial Cells.Biomolecules · 2026Review
- Mitochondrial Cristae Morphology Reflecting Metabolism, Superoxide Formation, Redox Homeostasis, and Pathology.Antioxidants & redox signaling · 2023Review
- The Role of Mitochondria in Mediation of Skeletal Muscle Repair.Muscles (Basel, Switzerland) · 2023Review
- Age-Related Dysfunction in Proteostasis and Cellular Quality Control in the Development of Sarcopenia.Cells · 2023Review
- Disturb mitochondrial associated proteostasis: Neurodegeneration and imperfect ageing.Frontiers in cell and developmental biology · 2023Review
- Prospects for the Development of Pink1 and Parkin Activators for the Treatment of Parkinson's Disease.Pharmaceutics · 2022Review
- Review
- LETM1: A Single Entity With Diverse Impact on Mitochondrial Metabolism and Cellular Signaling.Frontiers in physiology · 2021Review
- Light Microscopy of Mitochondria at the Nanoscale.Annual review of biophysics · 2020Review
- Improved spatial resolution by induced live cell and organelle swelling in hypotonic solutions.Scientific reports · 2019Article
- MICU1 controls cristae junction and spatially anchors mitochondrial CaNature communications · 2019Article
- Sensory neuropathy and nociception in rodent models of Parkinson's disease.Disease models & mechanisms · 2019Review
- A nanoscale, multi-parametric flow cytometry-based platform to study mitochondrial heterogeneity and mitochondrial DNA dynamics.Communications biology · 2019Article
- Three human aminoacyl-tRNA synthetases have distinct sub-mitochondrial localizations that are unaffected by disease-associated mutations.The Journal of biological chemistry · 2018Article
- Hypertonia-linked protein Trak1 functions with mitofusins to promote mitochondrial tethering and fusion.Protein & cell · 2018Article
- PINK1-mediated phosphorylation of LETM1 regulates mitochondrial calcium transport and protects neurons against mitochondrial stress.Nature communications · 2017Article
- Past, present, and emerging roles of mitochondrial heat shock protein TRAP1 in the metabolism and regulation of cancer stem cells.Cell stress & chaperones · 2016Review
- Ubiquitin phosphorylation in Parkinson's disease: Implications for pathogenesis and treatment.Translational neurodegeneration · 2016Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in mitochondrial kinase PINK1 cause Parkinson disease (PD), but the submitochondrial site(s) of PINK1 action remains unclear. Here, we report that three-dimensional structured illumination microscopy (3D-SIM) enables super-resolution imaging of protein submitochondrial localization. Dual-color 3D-SIM imaging analysis revealed that PINK1 resides in the cristae membrane and intracristae space but not on the outer mitochondrial membrane (OMM) of healthy mitochondria. Under normal physiological conditions, PINK1 colocalizes with its substrate TRAP1 in the cristae membrane and intracristae space. In response to mitochondrial depolarization, PINK1, but not TRAP1, translocates to the OMM. The PINK1 translocation to the OMM of depolarized mitochondria is independent of new protein synthesis and requires combined action of PINK1 transmembrane domain and C-terminal region. We found that mitochondrial depolarization-induced PINK1 OMM translocation is required for recruitment of parkin to the OMM of damaged mitochondria. Our findings suggest that differential submitochondrial localization of PINK1 serves as a molecular switch for mediating two distinct mitochondrial signaling pathways in maintenance of mitochondrial homeostasis. Furthermore, our study provides evidence for the involvement of deregulated PINK1 submitochondrial localization in PD pathogenesis.
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