ArticleDevelopment (Cambridge, England)2023
UNC-116 and UNC-16 function with the NEKL-3 kinase to promote axon targeting.
Article in Development (Cambridge, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Auxin-inducible degradation of UNC-116 in C. elegans inhibits bidirectional dense core vesicle transport and worm locomotion on different timescales.Journal of cell science · 2026Article
- Integrating endogenous TurboID and data-independent acquisition mass spectrometry for in vivo proximity labeling.The EMBO journal · 2026Article
- Phosphorylation-dependent regional motility of the ciliary kinesin OSM-3.The Journal of cell biology · 2025Article
- Article
- Autism candidate genebioRxiv : the preprint server for biology · 2024Article
- Molecular regulation of axon termination in mechanosensory neurons.Development (Cambridge, England) · 2024Review
- Article
- UNC-16 interacts with LRK-1 and WDFY-3 to regulate the termination of axon growth.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
KIF5C is a kinesin-1 heavy chain that has been associated with neurodevelopmental disorders. Although the roles of kinesin-1 in axon transport are well known, little is known about how it regulates axon targeting. We report that UNC-116/KIF5C functions with the NEKL-3/NEK6/7 kinase to promote axon targeting in Caenorhabditis elegans. Loss of UNC-116 causes the axon to overshoot its target and UNC-116 gain-of-function causes premature axon termination. We find that loss of the UNC-16/JIP3 kinesin-1 cargo adaptor disrupts axon termination, but loss of kinesin-1 light chain function does not affect axon termination. Genetic analysis indicates that UNC-16 functions with the NEKL-3 kinase to promote axon termination. Consistent with this observation, imaging experiments indicate that loss of UNC-16 and UNC-116 disrupt localization of NEKL-3 in the axon. Moreover, genetic interactions suggest that NEKL-3 promotes axon termination by functioning with RPM-1, a ubiquitin ligase that regulates microtubule stability in the growth cone. These observations support a model where UNC-116 functions with UNC-16 to promote localization of NEKL-3 in the axon. NEKL-3, in turn, functions with the RPM-1 ubiquitin ligase to promote axon termination.
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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.