ArticlePloS one2017
ROS regulation of axonal mitochondrial transport is mediated by Ca2+ and JNK in Drosophila.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- Spatial and morphological organization of mitochondria in neurons across a connectome.Science (New York, N.Y.) · 2026Article
- Silica Nanoparticles Induce BV-2 Cells Autophagy Via activation of NLRP3 inflammasome and CaMKK2 Signaling Pathways.Molecular neurobiology · 2026Article
- Amyotrophic Lateral Sclerosis With Concurrent LHON-associated m.14484T>C Mutation: A Case Report and Literature Review.Revista de neurologia · 2025Review
- Polar cell membrane nanotubes containing microtubules and acidic vesicles render Drosophila eggs fertile.PLoS biology · 2025Article
- Exploring mitochondrial dynamics and localization under cellular stress: A comprehensive insight.Journal of biosciences · 2025Review
- Ultrasound-Targeted Nanobubbles Codelivering NKP-1339 and miR-142-5p for Synergistic Mitochondrial Immunogenic Cell Death and PD-L1 Inhibition in Cancer Therapy.Biomaterials research · 2025Article
- Recent advances in mitochondrial transplantation to treat disease.Biomaterials translational · 2025Review
- Puckered and JNK signaling in pioneer neurons coordinates the motor activity of the Drosophila embryo.Nature communications · 2023Article
- Highly Specialized Mechanisms for Mitochondrial Transport in Neurons: From Intracellular Mobility to Intercellular Transfer of Mitochondria.Biomolecules · 2023Review
- Mitofusin 2 Sustains the Axonal Mitochondrial Network to Support Presynaptic CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Downregulation of oxidative stress-mediated glial innate immune response suppresses seizures in a fly epilepsy model.Cell reports · 2023Article
- How neurons maintain their axons long-term: an integrated view of axon biology and pathology.Frontiers in neuroscience · 2023Review
- Mitochondrial heterogeneity and homeostasis through the lens of a neuron.Nature metabolism · 2022Review
- Programming axonal mitochondrial maintenance and bioenergetics in neurodegeneration and regeneration.Neuron · 2022Review
- Drosophila Primary Neuronal Cultures as a Useful Cellular Model to Study and Image Axonal Transport.Methods in molecular biology (Clifton, N.J.) · 2022Article
- In Vivo Live Imaging of Axonal Transport in Developing Zebrafish Axons.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Perisciatic Nerve Dexmedetomidine Alleviates Spinal Oxidative Stress and Improves Peripheral Mitochondrial Dynamic Equilibrium in a Neuropathic Pain Mouse Model in an AMPK-Dependent Manner.Disease markers · 2022Article
- Pathophysiology of neurodegenerative diseases: An interplay among axonal transport failure, oxidative stress, and inflammation?Seminars in immunology · 2022Review
- Treatment of ischemic stroke with modified mesenchymal stem cells.International journal of medical sciences · 2022Review
- Circ-Hdgfrp3 shuttles along neurites and is trapped in aggregates formed by ALS-associated mutant FUS.iScience · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria perform critical functions including aerobic ATP production and calcium (Ca2+) homeostasis, but are also a major source of reactive oxygen species (ROS) production. To maintain cellular function and survival in neurons, mitochondria are transported along axons, and accumulate in regions with high demand for their functions. Oxidative stress and abnormal mitochondrial axonal transport are associated with neurodegenerative disorders. However, we know little about the connection between these two. Using the Drosophila third instar larval nervous system as the in vivo model, we found that ROS inhibited mitochondrial axonal transport more specifically, primarily due to reduced flux and velocity, but did not affect transport of other organelles. To understand the mechanisms underlying these effects, we examined Ca2+ levels and the JNK (c-Jun N-terminal Kinase) pathway, which have been shown to regulate mitochondrial transport and general fast axonal transport, respectively. We found that elevated ROS increased Ca2+ levels, and that experimental reduction of Ca2+ to physiological levels rescued ROS-induced defects in mitochondrial transport in primary neuron cell cultures. In addition, in vivo activation of the JNK pathway reduced mitochondrial flux and velocities, while JNK knockdown partially rescued ROS-induced defects in the anterograde direction. We conclude that ROS have the capacity to regulate mitochondrial traffic, and that Ca2+ and JNK signaling play roles in mediating these effects. In addition to transport defects, ROS produces imbalances in mitochondrial fission-fusion and metabolic state, indicating that mitochondrial transport, fission-fusion steady state, and metabolic state are closely interrelated in the response to ROS.
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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.