ArticleMolecular biology of the cell1999
Cytoplasmic dynein, the dynactin complex, and kinesin are interdependent and essential for fast axonal transport.
Article in Molecular biology of the cell, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 182 papers.
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Who cites it
182 citing papers in PubMed, 366 citations in OpenAlex.
- Evolutionary genomic basis of mimicry diversity of Epicopeiidae moths.Molecular biology and evolution · 2026Article
- Synaptic-mitochondrial transport: mechanisms in neural adaptation and degeneration.Molecular and cellular biochemistry · 2025Review
- KIF1C activates and extends dynein movement through the FHF cargo adapter.Nature structural & molecular biology · 2025Article
- Mitochondrial dysfunction in Alzheimer's disease: Guiding the path to targeted therapies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Dynein-driven regulation of postsynaptic membrane architecture and synaptic function.Journal of cell science · 2025Article
- A force-sensitive mutation reveals a non-canonical role for dynein in anaphase progression.The Journal of cell biology · 2024Article
- In vivo optogenetic manipulations of endogenous proteins reveal spatiotemporal roles of microtubule and kinesin in dendrite patterning.Science advances · 2024Article
- Optogenetic control of kinesin-1, -2, -3 and dynein reveals their specific roles in vesicular transport.Cell reports · 2024Article
- The ALS-associated KIF5A P986L variant is not pathogenic for Drosophila motoneurons.Scientific reports · 2024Article
- PKA Activity-Driven Modulation of Bidirectional Long-Distance transport of Lysosomal vesicles During Synapse Maintenance.bioRxiv : the preprint server for biology · 2024Article
- Dynein and dynactin move long-range but are delivered separately to the axon tip.The Journal of cell biology · 2024Article
- Axonal transport of autophagosomes is regulated by dynein activators JIP3/JIP4 and ARF/RAB GTPases.The Journal of cell biology · 2023Article
- ALS-Associated KIF5A Mutation Causes Locomotor Deficits Associated with Cytoplasmic Inclusions, Alterations of Neuromuscular Junctions, and Motor Neuron Loss.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Speech- and language-linked FOXP2 mutation targets protein motors in striatal neurons.Brain : a journal of neurology · 2023Article
- Compartment specific mitochondrial dysfunction in Drosophila knock-in model of ALS reversed by altered gene expression of OXPHOS subunits and pro-fission factor Drp1.Molecular and cellular neurosciences · 2023Article
- Axonal transport during injury on a theoretical axon.Frontiers in cellular neuroscience · 2023Article
- Selective motor activation in organelle transport along axons.Nature reviews. Molecular cell biology · 2022Review
- Article
- Simple to Complex: The Role of Actin and Microtubules in Mitochondrial Dynamics in Amoeba, Yeast, and Mammalian Cells.International journal of molecular sciences · 2022Review
- Axon Biology in ALS: Mechanisms of Axon Degeneration and Prospects for Therapy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Review
122 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
In axons, organelles move away from (anterograde) and toward (retrograde) the cell body along microtubules. Previous studies have provided compelling evidence that conventional kinesin is a major motor for anterograde fast axonal transport. It is reasonable to expect that cytoplasmic dynein is a fast retrograde motor, but relatively few tests of dynein function have been reported with neurons of intact organisms. In extruded axoplasm, antibody disruption of kinesin or the dynactin complex (a dynein activator) inhibits both retrograde and anterograde transport. We have tested the functions of the cytoplasmic dynein heavy chain (cDhc64C) and the p150(Glued) (Glued) component of the dynactin complex with the use of genetic techniques in Drosophila. cDhc64C and Glued mutations disrupt fast organelle transport in both directions. The mutant phenotypes, larval posterior paralysis and axonal swellings filled with retrograde and anterograde cargoes, were similar to those caused by kinesin mutations. Why do specific disruptions of unidirectional motor systems cause bidirectional defects? Direct protein interactions of kinesin with dynein heavy chain and p150(Glued) were not detected. However, strong dominant genetic interactions between kinesin, dynein, and dynactin complex mutations in axonal transport were observed. The genetic interactions between kinesin and either Glued or cDhc64C mutations were stronger than those between Glued and cDhc64C mutations themselves. The shared bidirectional disruption phenotypes and the dominant genetic interactions demonstrate that cytoplasmic dynein, the dynactin complex, and conventional kinesin are interdependent in fast axonal transport.
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