ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Loss of the spectraplakin short stop activates the DLK injury response pathway in Drosophila.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 82 citations in OpenAlex.
- Article
- A tubulin-MAPKKK pathway engages tubulin isotype interaction for neuroprotection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Drosophila Topoisomerase 3β binds to mRNAs in vivo, contributes to their localization and stability, and counteracts premature aging.PloS one · 2025Article
- Article
- A miR-383-5p Signaling Hub Coordinates the Axon Regeneration Response to Inflammation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Remyelination protects neurons from DLK-mediated neurodegeneration.Nature communications · 2024Article
- Microtubules, Membranes, and Movement: New Roles for Stathmin-2 in Axon Integrity.Journal of neuroscience research · 2024Review
- Remyelination protects neurons from DLK-mediated neurodegeneration.bioRxiv : the preprint server for biology · 2024Article
- Review
- Neural regeneration in the human central nervous system-from understanding the underlying mechanisms to developing treatments. Where do we stand today?Frontiers in neurology · 2024Review
- The response of Dual-leucine zipper kinase (DLK) to nocodazole: Evidence for a homeostatic cytoskeletal repair mechanism.PloS one · 2024Article
- The Stathmin-2 membrane-targeting domain is required for axon protection and regulated degradation by DLK signaling.The Journal of biological chemistry · 2023Article
- Molecular mechanisms of neurite regeneration and repair: insights from C. elegans and Drosophila.Cell regeneration (London, England) · 2023Review
- Axonal Regeneration: Underlying Molecular Mechanisms and Potential Therapeutic Targets.Biomedicines · 2022Review
- Distinct developmental and degenerative functions of SARM1 require NAD+ hydrolase activity.PLoS genetics · 2022Article
- Protein phosphatase 2A restrains DLK signaling to promote proper Drosophila synaptic development and mammalian cortical neuron survival.Neurobiology of disease · 2022Article
- The Role of Spastin in Axon Biology.Frontiers in cell and developmental biology · 2022Review
- Article
- Integrated analysis of the aging brain transcriptome and proteome in tauopathy.Molecular neurodegeneration · 2020Article
- Structural and Functional Plasticity in the Regenerating Olfactory System of the Migratory Locust.Frontiers in physiology · 2020Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The MAPKKK dual leucine zipper-containing kinase (DLK, Wallenda in Drosophila) is an evolutionarily conserved component of the axonal injury response pathway. After nerve injury, DLK promotes degeneration of distal axons and regeneration of proximal axons. This dual role in coordinating degeneration and regeneration suggests that DLK may be a sensor of axon injury, and so understanding how DLK is activated is important. Two mechanisms are known to activate DLK. First, increasing the levels of DLK via overexpression or loss of the PHR ubiquitin ligases that target DLK activate DLK signaling. Second, in Caenorhabditis elegans, a calcium-dependent mechanism, can activate DLK. Here we describe a new mechanism that activates DLK in Drosophila: loss of the spectraplakin short stop (shot). In a genetic screen for mutants with defective neuromuscular junction development, we identify a hypomorphic allele of shot that displays synaptic terminal overgrowth and a precocious regenerative response to nerve injury. We demonstrate that both phenotypes are the result of overactivation of the DLK signaling pathway. We further show that, unlike mutations in the PHR ligase Highwire, loss of function of shot activates DLK without a concomitant increase in the levels of DLK. As a spectraplakin, Shot binds to both actin and microtubules and promotes cytoskeletal stability. The DLK pathway is also activated by downregulation of the TCP1 chaperonin complex, whose normal function is to promote cytoskeletal stability. These findings support the model that DLK is activated by cytoskeletal instability, which is a shared feature of both spectraplakin mutants and injured axons.
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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.