ArticleThe Journal of cell biology2024
Actomyosin-II protects axons from degeneration induced by mild mechanical stress.
Article in The Journal of cell biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Fine-Tuned Regulation of mRNA Translation and Transport by STAU2 Condensate Facilitates Neuronal Development and Plasticity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Axonopathy: mechanisms and potential therapeutic targets for neurodegenerative diseases.Translational neurodegeneration · 2026Review
- Article
- Article
- Annexin A7 enhances TIA1 axonal trafficking to counteract pathological aggregation in neurons.The EMBO journal · 2025Article
- Nonmuscle myosin II regulates presynaptic actin and neuronal mechanobiology in Drosophila.The Journal of cell biology · 2025Article
- Monkeypox virus spreads from cell-to-cell and leads to neuronal death in human neural organoids.Nature communications · 2025Article
- Myosin 2 - A general contractor for the cytoskeleton.Current opinion in cell biology · 2025Review
- Article
- Cellular mechanisms of traumatic brain injury.npj biological physics and mechanics · 2025Review
- Super-resolution imaging of the neuronal cytoskeleton.Npj imaging · 2024Review
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Authors and funding
15 authors.
Funding
Abstract
Whether, to what extent, and how the axons in the central nervous system (CNS) can withstand sudden mechanical impacts remain unclear. By using a microfluidic device to apply controlled transverse mechanical stress to axons, we determined the stress levels that most axons can withstand and explored their instant responses at nanoscale resolution. We found mild stress triggers a highly reversible, rapid axon beading response, driven by actomyosin-II-dependent dynamic diameter modulations. This mechanism contributes to hindering the long-range spread of stress-induced Ca2+ elevations into non-stressed neuronal regions. Through pharmacological and molecular manipulations in vitro, we found that actomyosin-II inactivation diminishes the reversible beading process, fostering progressive Ca2+ spreading and thereby increasing acute axonal degeneration in stressed axons. Conversely, upregulating actomyosin-II activity prevents the progression of initial injury, protecting stressed axons from acute degeneration both in vitro and in vivo. Our study unveils the periodic actomyosin-II in axon shafts cortex as a novel protective mechanism, shielding neurons from detrimental effects caused by mechanical stress.
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Registered trials
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