ArticleGenetics2021
UNC-16 alters DLK-1 localization and negatively regulates actin and microtubule dynamics in Caenorhabditis elegans regenerating neurons.
Article in Genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Multiple regulators constrain the abundance of Caenorhabditis elegans DLK-1 in ciliated sensory neurons.G3 (Bethesda, Md.) · 2025Article
- Disruptions in axonal lysosome transport and its contribution to neurological disease.Current opinion in cell biology · 2024Review
- Molecular mechanisms of neurite regeneration and repair: insights from C. elegans and Drosophila.Cell regeneration (London, England) · 2023Review
- JIP3 links lysosome transport to regulation of multiple components of the axonal cytoskeleton.Communications biology · 2022Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Neuronal regeneration after injury depends on the intrinsic growth potential of neurons. Our study shows that UNC-16, a Caenorhabditis elegans JIP3 homolog, inhibits axonal regeneration by regulating initiation and rate of regrowth. This occurs through the inhibition of the regeneration-promoting activity of the long isoform of DLK-1 and independently of the inhibitory short isoform of DLK-1. We show that UNC-16 promotes DLK-1 punctate localization in a concentration-dependent manner limiting the availability of the long isoform of DLK-1 at the cut site, minutes after injury. UNC-16 negatively regulates actin dynamics through DLK-1 and microtubule dynamics partially via DLK-1. We show that post-injury cytoskeletal dynamics in unc-16 mutants are also partially dependent on CEBP-1. The faster regeneration seen in unc-16 mutants does not lead to functional recovery. Our data suggest that the inhibitory control by UNC-16 and the short isoform of DLK-1 balances the intrinsic growth-promoting function of the long isoform of DLK-1 in vivo. We propose a model where UNC-16's inhibitory role in regeneration occurs through both a tight temporal and spatial control of DLK-1 and cytoskeletal dynamics.
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