Kinesin-2 is a motor for late endosomes and lysosomes
Abstract
The bidirectional nature of late endosome/lysosome movement suggests involvement of at least two distinct motors, one minus‐end directed and one plus‐end directed. Previous work has identified dynein as the minus‐end‐directed motor for late endosome/lysosome localization and dynamics. Conventional kinesin (kinesin‐1) has been implicated in plus‐end‐directed late endosome/lysosome movement, but other kinesin family members may also be involved. Kinesin‐2 is known to drive the movement of pigment granules, a type of lysosomally derived organelle, and was recently found to be associated with purified late endosomes. To determine whether kinesin‐2 might also power endosome movement in non‐pigmented cells, we overexpressed dominant negative forms of the KIF3A motor subunit and KAP3 accessory subunit and knocked down KAP3 levels using RNAi. We found kinesin‐2 to be required for the normal steady‐state localization of late endosomes/lysosomes but not early endosomes or recycling endosomes. Despite the abnormal subcellular distribution of late endosomes/lysosomes, the uptake and trafficking of molecules through the conventional endocytic pathway appeared to be unaffected. The slow time–course of inhibition suggests that both kinesin‐2 itself and its attachment to membranes do not turn over quickly.
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Lysosomes are transported by teams of kinesin-1, -2, and -3 and dynein motors.
“lysosomes are transported by teams of kinesin-1, -2, and -3 and dynein motors”
From Tau hyperphosphorylation impairs cooperative binding to microtubules and perturbs organelle trafficking in neurons (2026) · cites this paper as Brown et al., 2005
Cites
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BackgroundThe Molecular Motor Toolbox for Intracellular Transport
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Kinesin superfamily motor proteins and intracellular transport
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Beaudet, D., Berger, C. L., & Hendricks, A. G. (2026) · eLife · doi:10.7554/elife.110011
- Authors
- Brown, C. L., Maier, K. C., Stauber, T., Ginkel, L. M., Wordeman, L., Vernos, I., & Schroer, T. A.
- Affiliations
- Johns Hopkins University (US)
- European Molecular Biology Laboratory (DE)
- University of Washington (US)
- Corresponding author
- Schroer, Trina A.
- Venue
- Traffic
- Publisher
- Wiley
- Published
- 2005-10-18
- Volume
- 6
- Issue
- 12
- Pages
- 1114-1124
- ISSN
- 1398-9219 (ISSN-L)
- 1600-0854
- OpenAlex
- W1715906171
- Cited by
- 140
- References
- 4
- Citations by year
- 2026: 4 · 2024: 3 · 2023: 3 · 2022: 4 · 2021: 4 · 2020: 7 · 2019: 8 · 2018: 4 · 2017: 8 · 2016: 8 · 2015: 6 · 2014: 8 · 2013: 6 · 2012: 15
- FWCI
- 2.92
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Traffic (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of General Medical Sciences (R01GM044589)
- National Institute of Diabetes and Digestive and Kidney Diseases (P01DK044375)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- kinesin-2, late endosomes, lysosomes, endosome motility, KIF3A, RNAi knockdown, endocytic pathway, dynein
- MeSH terms
- Animals, Chlorocebus aethiops, HeLa Cells, Humans, Lysosomes, Microtubule-Associated Proteins, Endosomes, Kinesins, COS Cells
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