ArticlePLoS genetics2016
Mitochondria and Caspases Tune Nmnat-Mediated Stabilization to Promote Axon Regeneration.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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Who cites it
32 citing papers in PubMed, 37 citations in OpenAlex.
- Identification of a cytosol-to-nucleus feedback loop that regulates neuronal microtubule nucleation.The Journal of cell biology · 2026Article
- DLK orchestrates a modular transcriptional response to axon injury with separate roles for Fos and Jun.PLoS genetics · 2025Article
- SARM1: The Checkpoint of Axonal Degeneration in the Nervous System Disorders.Molecular neurobiology · 2025Review
- Study of Axonal Injury and Degeneration inCold Spring Harbor protocols · 2025Article
- Nerve growth factor signaling tunes axon maintenance protein abundance and kinetics of Wallerian degeneration.Molecular biology of the cell · 2025Article
- Endocytosis of Wnt ligands from surrounding epithelial cells positions microtubule nucleation sites at dendrite branch points.PLoS biology · 2025Article
- Nerve Growth Factor Signaling Tunes Axon Maintenance Protein Abundance and Kinetics of Wallerian Degeneration.bioRxiv : the preprint server for biology · 2025Article
- DLK-dependent axonal mitochondrial fission drives degeneration after axotomy.Nature communications · 2024Article
- DLK-dependent axonal mitochondrial fission drives degeneration following axotomy.bioRxiv : the preprint server for biology · 2024Article
- The MAP3Ks DLK and LZK Direct Diverse Responses to Axon Damage in Zebrafish Peripheral Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Insights into nervous system repair from the fruit fly.Neuronal signaling · 2022Review
- Multifaceted roles of SARM1 in axon degeneration and signaling.Frontiers in cellular neuroscience · 2022Review
- Non-Apoptotic Role of Apoptotic Caspases in theFrontiers in cell and developmental biology · 2022Review
- Parallels between the Developing Vascular and Neural Systems: Signaling Pathways and Future Perspectives for Regenerative Medicine.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Review
- To nucleate or not, that is the question in neurons.Neuroscience letters · 2021Review
- Microtubule dynamics in healthy and injured neurons.Developmental neurobiology · 2021Review
- Pathogenic role of delta 2 tubulin in bortezomib-induced peripheral neuropathy.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- NADFrontiers in molecular biosciences · 2021Review
- Kinetochore proteins suppress neuronal microtubule dynamics and promote dendrite regeneration.Molecular biology of the cell · 2020Article
- Effects of NADBiomolecules · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Axon injury can lead to several cell survival responses including increased stability and axon regeneration. Using an accessible Drosophila model system, we investigated the regulation of injury responses and their relationship. Axon injury stabilizes the rest of the cell, including the entire dendrite arbor. After axon injury we found mitochondrial fission in dendrites was upregulated, and that reducing fission increased stabilization or neuroprotection (NP). Thus axon injury seems to both turn on NP, but also dampen it by activating mitochondrial fission. We also identified caspases as negative regulators of axon injury-mediated NP, so mitochondrial fission could control NP through caspase activation. In addition to negative regulators of NP, we found that nicotinamide mononucleotide adenylyltransferase (Nmnat) is absolutely required for this type of NP. Increased microtubule dynamics, which has previously been associated with NP, required Nmnat. Indeed Nmnat overexpression was sufficient to induce NP and increase microtubule dynamics in the absence of axon injury. DLK, JNK and fos were also required for NP. Because NP occurs before axon regeneration, and NP seems to be actively downregulated, we tested whether excessive NP might inhibit regeneration. Indeed both Nmnat overexpression and caspase reduction reduced regeneration. In addition, overexpression of fos or JNK extended the timecourse of NP and dampened regeneration in a Nmnat-dependent manner. These data suggest that NP and regeneration are conflicting responses to axon injury, and that therapeutic strategies that boost NP may reduce regeneration.
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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.