ArticleThe EMBO journal2024
Neurons dispose of hyperactive kinesin into glial cells for clearance.
Article in The EMBO journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Heterotrimeric kinesin-2 autoinhibition mediated by interactions of the CC2 and proximal tail domains with the motor domains is essential for cilium formation and maintenance.bioRxiv : the preprint server for biology · 2026Article
- Joubert syndrome 26 protein enforces compartmentalized motility of a ciliary kinesin.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- C. elegans: An elegant experimental system for the study of cilia biology.Seminars in cell & developmental biology · 2025Review
- Article
- A mutual co-recognition mechanism ensures the proper assembly of heterotrimeric kinesin-2 for intraflagellar transport.Nature communications · 2025Article
- Phosphorylation-dependent regional motility of the ciliary kinesin OSM-3.The Journal of cell biology · 2025Article
- Article
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Authors and funding
14 authors.
Funding
Abstract
Microtubule-based kinesin motor proteins are crucial for intracellular transport, but their hyperactivation can be detrimental for cellular functions. This study investigated the impact of a constitutively active ciliary kinesin mutant, OSM-3CA, on sensory cilia in C. elegans. Surprisingly, we found that OSM-3CA was absent from cilia but underwent disposal through membrane abscission at the tips of aberrant neurites. Neighboring glial cells engulf and eliminate the released OSM-3CA, a process that depends on the engulfment receptor CED-1. Through genetic suppressor screens, we identified intragenic mutations in the OSM-3CA motor domain and mutations inhibiting the ciliary kinase DYF-5, both of which restored normal cilia in OSM-3CA-expressing animals. We showed that conformational changes in OSM-3CA prevent its entry into cilia, and OSM-3CA disposal requires its hyperactivity. Finally, we provide evidence that neurons also dispose of hyperactive kinesin-1 resulting from a clinic variant associated with amyotrophic lateral sclerosis, suggesting a widespread mechanism for regulating hyperactive kinesins.
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Registered trials
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