ArticleScientific reports2018
UNC-16/JIP3 and UNC-76/FEZ1 limit the density of mitochondria in C. elegans neurons by maintaining the balance of anterograde and retrograde mitochondrial transport.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- Non-Mammalian Models for Mitochondria Research in CNS Disorders.Biomolecules · 2026Review
- Auxin-inducible degradation of UNC-116 in C. elegans inhibits bidirectional dense core vesicle transport and worm locomotion on different timescales.Journal of cell science · 2026Article
- Mitochondria transported by Kinesin-3 prevent localized calcium spiking to inhibit caspase-dependent specialized cell death.Current biology : CB · 2025Article
- Sequelae and reversal of age-dependent alterations in mitochondrial dynamics via autophagy enhancement in reprogrammed human neurons.bioRxiv : the preprint server for biology · 2025Article
- The role of kinesin-1 in neuronal dense core vesicle transport, locomotion and lifespan regulation in C. elegans.Journal of cell science · 2024Article
- Axonal mitochondria regulate gentle touch response through control of axonal actin dynamics.bioRxiv : the preprint server for biology · 2024Article
- Article
- Polarized localization of kinesin-1 and RIC-7 drives axonal mitochondria anterograde transport.The Journal of cell biology · 2024Article
- UNC-16 interacts with LRK-1 and WDFY-3 to regulate the termination of axon growth.bioRxiv : the preprint server for biology · 2024Article
- A kinesin-1 adaptor complex controls bimodal slow axonal transport of spectrin in Caenorhabditis elegans.Developmental cell · 2023Article
- UNC-116 and UNC-16 function with the NEKL-3 kinase to promote axon targeting.Development (Cambridge, England) · 2023Article
- JIP3 interacts with dynein and kinesin-1 to regulate bidirectional organelle transport.The Journal of cell biology · 2022Article
- The importance of fasciculation and elongation protein zeta-1 in neural circuit establishment and neurological disorders.Neural regeneration research · 2022Review
- Article
- JIP3 links lysosome transport to regulation of multiple components of the axonal cytoskeleton.Communications biology · 2022Article
- Imaging Intracellular Trafficking in Neurons of C. elegans.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Increased mitochondrial calcium uptake and concomitant mitochondrial activity by presenilin loss promotes mTORC1 signaling to drive neurodegeneration.Aging cell · 2021Article
- CRMP/UNC-33 organizes microtubule bundles for KIF5-mediated mitochondrial distribution to axon.PLoS genetics · 2021Article
- Touch-induced mechanical strain in somatosensory neurons is independent of extracellular matrix mutations inMolecular biology of the cell · 2020Article
- Structural characterization of the RH1-LZI tandem of JIP3/4 highlights RH1 domains as a cytoskeletal motor-binding motif.Scientific reports · 2019Article
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Authors and funding
8 authors at 3 institutions in 1 country.
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Abstract
We investigate the role of axonal transport in regulating neuronal mitochondrial density. We show that the density of mitochondria in the touch receptor neuron (TRN) of adult Caenorhabditis elegans is constant. Mitochondrial density and transport are controlled both by the Kinesin heavy chain and the Dynein-Dynactin complex. However, unlike in other models, the presence of mitochondria in C. elegans TRNs depends on a Kinesin light chain as well. Mutants in the three C. elegans miro genes do not alter mitochondrial density in the TRNs. Mutants in the Kinesin-1 associated proteins, UNC-16/JIP3 and UNC-76/FEZ1, show increased mitochondrial density and also have elevated levels of both the Kinesin Heavy and Light Chains in neurons. Genetic analyses suggest that, the increased mitochondrial density at the distal end of the neuronal process in unc-16 and unc-76 depends partly on Dynein. We observe a net anterograde bias in the ratio of anterograde to retrograde mitochondrial flux in the neuronal processes of unc-16 and unc-76, likely due to both increased Kinesin-1 and decreased Dynein in the neuronal processes. Our study shows that UNC-16 and UNC-76 indirectly limit mitochondrial density in the neuronal process by maintaining a balance in anterograde and retrograde mitochondrial axonal transport.
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