Kinesin Light Chains Are Essential for Axonal Transport in Drosophila
Open accessAbstract
Kinesin is a heterotetramer composed of two 115-kD heavy chains and two 58-kD light chains. The microtubule motor activity of kinesin is performed by the heavy chains, but the functions of the light chains are poorly understood. Mutations were generated in the Drosophila gene Kinesin light chain (Klc), and the phenotypic consequences of loss of Klc function were analyzed at the behavioral and cellular levels. Loss of Klc function results in progressive lethargy, crawling defects, and paralysis followed by death at the end of the second larval instar. Klc mutant axons contain large aggregates of membranous organelles in segmental nerve axons. These aggregates, or organelle jams (Hurd, D.D., and W.M. Saxton. 1996. Genetics. 144: 1075-1085), contain synaptic vesicle precursors as well as organelles that may be transported by kinesin, kinesin-like protein 68D, and cytoplasmic dynein, thus providing evidence that the loss of Klc function blocks multiple pathways of axonal transport. The similarity of the Klc and Khc (. Cell 64:1093-1102; Hurd, D.D., and W.M. Saxton. 1996. Genetics 144: 1075-1085) mutant phenotypes indicates that KLC is essential for kinesin function, perhaps by tethering KHC to intracellular cargos or by activating the kinesin motor.
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Mutants lacking KLC in Drosophila melanogaster exhibit neuronal phenotypes similar to those seen when KHC is removed.
“Mutants lacking KLC in Drosophila melanogaster (Gindhart et al. 1998) exhibit neuronal phenotypes similar to that seen when KHC is removed.”
From Defective kinesin heavy chain behavior in mouse kinesin light chain mutants (1999) · cites this paper as Gindhart et al. 1998
Both KLC and KHC mutants in Drosophila exhibit membranous clogs in the segmental nerves.
“In fact, both KLC and KHC mutants in Drosophila exhibit membranous clogs in the segmental nerves (Hurd and Saxton 1996; Gindhart et al. 1998).”
From Defective kinesin heavy chain behavior in mouse kinesin light chain mutants (1999) · cites this paper as Gindhart et al. 1998
Results of disruption of KLC in Drosophila and mice suggest an essential role for KLC in kinesin function.
“However, the results of disruption of KLC in Drosophila and mice suggest an essential role for KLC in kinesin function (Gindhart et al. 1998).”
From Cargo of kinesin identified as JIP scaffolding proteins and associated signaling molecules (2001) · cites this paper as Gindhart et al. 1998
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Drosophila VAP-33A Directs Bouton Formation at Neuromuscular Junctions in a Dosage-Dependent Manner
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UNC-51/ATG1 kinase regulates axonal transport by mediating motor–cargo assemblyPreprint
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Kinesin-II Is Required for Axonal Transport of Choline Acetyltransferase in Drosophila
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Self-citationDynein light chain regulates axonal trafficking and synaptic levels of Bassoon
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Sunday Driver/JIP3 binds kinesin heavy chain directly and enhances its motility
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Self-citationHigh‐resolution imaging demonstrates dynein‐based vesicular transport of activated trk receptors
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Functional anatomy of the kinesin molecule in vivo
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Jia, Z., Wang, M., Li, S., Li, X., Bai, X., Xu, Z., Yang, Y. Y., Li, B., Li, Y., & Wu, H. (2018) · Cell Death and Disease · doi:10.1038/s41419-017-0094-4 · Cited by 35 · see citing works
KAP, the Accessory Subunit of Kinesin-2, Binds the Predicted Coiled-Coil Stalk of the Motor Subunits
Doodhi, H., Ghosal, D., Krishnamurthy, M., Jana, S. C., Shamala, D., Bhaduri, A., Sowdhamini, R., & Ray, K. (2009) · Biochemistry · doi:10.1021/bi8018338 · Cited by 35 · see citing works
Wortman, J. C., Shrestha, U., Barry, D. M., Garcia, M. L., Gross, S. P., & Yu, C. C. (2014) · Biophysical Journal · doi:10.1016/j.bpj.2013.12.047 · Cited by 35 · see citing works
- Authors
- Gindhart, J. G., Desai, C. J., Beushausen, S., Zinn, K., & Goldstein, L. S. B.
- Affiliations
- California Institute of Technology (US)
- Venue
- The Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 1998-04-20
- Volume
- 141
- Issue
- 2
- Pages
- 443-454
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC2148443
- OpenAlex
- W2099198611
- Cited by
- 179
- References
- 105
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 2 · 2023: 2 · 2022: 4 · 2021: 2 · 2020: 2 · 2019: 3 · 2018: 6 · 2017: 9 · 2016: 3 · 2015: 5 · 2014: 8 · 2013: 7 · 2012: 10
- FWCI
- 4.32
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Cell Biology (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion, cc-by-nc-sa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Hereditary Neurological Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Keywords
- kinesin light chain, axonal transport, kinesin heavy chain, Drosophila, cytoplasmic dynein, cargo binding, paralysis, larval mortality
- MeSH terms
- Animals, Axonal Transport, Drosophila, Larva, Microtubule-Associated Proteins, Movement, Mutation, Nerve Tissue Proteins, Neurons, Paralysis, Phenotype, Kinesins, Genes, Insect, Animals, Genetically Modified
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