ArticlePLoS genetics2021
Motor domain-mediated autoinhibition dictates axonal transport by the kinesin UNC-104/KIF1A.
Article in PLoS genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- 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
- Rules of the road: how to turn off kinesin motors.The Biochemical journal · 2026Review
- Article
- The alpha tubulin acetyltransferasemicroPublication biology · 2025Article
- KLP-7/Kinesin-13 orchestrates axon-dendrite checkpoints for polarized trafficking in neurons.Molecular biology of the cell · 2024Article
- F-box protein FBXB-65 regulates anterograde transport of the kinesin-3 motor UNC-104 through a PTM near its cargo-binding PH domain.Journal of cell science · 2024Article
- A plant flavonol and genetic suppressors rescue a pathogenic mutation associated with kinesin in neurons.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Comparative analysis of twoeLife · 2024Article
- Article
- KIF1A-Associated Neurological Disorder: An Overview of a Rare Mutational Disease.Pharmaceuticals (Basel, Switzerland) · 2023Review
- How neurons maintain their axons long-term: an integrated view of axon biology and pathology.Frontiers in neuroscience · 2023Review
- The architecture of kinesin-3 KLP-6 reveals a multilevel-lockdown mechanism for autoinhibition.Nature communications · 2022Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The UNC-104/KIF1A motor is crucial for axonal transport of synaptic vesicles, but how the UNC-104/KIF1A motor is activated in vivo is not fully understood. Here, we identified point mutations located in the motor domain or the inhibitory CC1 domain, which resulted in gain-of-function alleles of unc-104 that exhibit hyperactive axonal transport and abnormal accumulation of synaptic vesicles. In contrast to the cell body localization of wild type motor, the mutant motors accumulate on neuronal processes. Once on the neuronal process, the mutant motors display dynamic movement similarly to wild type motors. The gain-of-function mutation on the motor domain leads to an active dimeric conformation, releasing the inhibitory CC1 region from the motor domain. Genetically engineered mutations in the motor domain or CC1 of UNC-104, which disrupt the autoinhibitory interface, also led to the gain of function and hyperactivation of axonal transport. Thus, the CC1/motor domain-mediated autoinhibition is crucial for UNC-104/KIF1A-mediated axonal transport in vivo.
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