ArticleThe Journal of cell biology2021
Pathogenic mutations in the kinesin-3 motor KIF1A diminish force generation and movement through allosteric mechanisms.
Article in The Journal of cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 99 citations in OpenAlex.
- Article
- KIF1A-mediated trafficking is required for neuronal autophagy in human neurons.bioRxiv : the preprint server for biology · 2026Article
- Article
- KLP-6 is a kinesin superfamily protein resistant to ADP inhibition.Communications biology · 2026Article
- Pathogenic KIF1A R350 mutations disrupt a conserved and conformation-dependent kinesin-tubulin salt bridge.Nature communications · 2026Article
- Stall force measurement of the kinesin-3 motor KIF1A using a programmable DNA origami nanospring.eLife · 2026Article
- Adaptor-mediated recruitment of three dyneins to dynactin enhances force generation.Nature cell biology · 2026Article
- DNA tensiometer reveals catch-bond detachment kinetics of kinesin-1, -2 and -3.bioRxiv : the preprint server for biology · 2025Article
- ALS Mutations Shift the Isoelectric Point of the KIF5A C Terminal Inducing Protein Aggregation and TDP-43 Mislocalization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Distinct Clinical Phenotypes in KIF1A-Associated Neurological Disorders Result from Different Amino Acid Substitutions at the Same Residue in KIF1A.Biomolecules · 2025Article
- KIF1C activates and extends dynein movement through the FHF cargo adapter.Nature structural & molecular biology · 2025Article
- Mechanism and regulation of kinesin motors.Nature reviews. Molecular cell biology · 2025Review
- Biased movement of monomeric kinesin-3 KLP-6 explained by a symmetric Brownian ratchet model.Biophysical journal · 2025Article
- Genotype-phenotype correlations in 18 European patients with heterozygousFrontiers in medicine · 2025Article
- Kinesin-14 HSET and KlpA are non-processive microtubule motors with load-dependent power strokes.Nature communications · 2024Article
- Cryo-EM unveils kinesin KIF1A's processivity mechanism and the impact of its pathogenic variant P305L.Nature communications · 2024Article
- A Model for Chemomechanical Coupling of Kinesin-3 Motor.Cellular and molecular bioengineering · 2024Article
- Cargo specificity, regulation, and therapeutic potential of cytoplasmic dynein.Experimental & molecular medicine · 2024Review
- Noncanonical interaction with microtubules via the N-terminal nonmotor domain is critical for the functions of a bidirectional kinesin.Science advances · 2024Article
- Comparative analysis of twoeLife · 2024Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The kinesin-3 motor KIF1A functions in neurons, where its fast and superprocessive motility facilitates long-distance transport, but little is known about its force-generating properties. Using optical tweezers, we demonstrate that KIF1A stalls at an opposing load of ~3 pN but more frequently detaches at lower forces. KIF1A rapidly reattaches to the microtubule to resume motion due to its class-specific K-loop, resulting in a unique clustering of force generation events. To test the importance of neck linker docking in KIF1A force generation, we introduced mutations linked to human neurodevelopmental disorders. Molecular dynamics simulations predict that V8M and Y89D mutations impair neck linker docking. Indeed, both mutations dramatically reduce the force generation of KIF1A but not the motor's ability to rapidly reattach to the microtubule. Although both mutations relieve autoinhibition of the full-length motor, the mutant motors display decreased velocities, run lengths, and landing rates and delayed cargo transport in cells. These results advance our understanding of how mutations in KIF1A can manifest in disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.