ArticleActa neuropathologica2016
Neurofilament depletion improves microtubule dynamics via modulation of Stat3/stathmin signaling.
Article in Acta neuropathologica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 31 citations in OpenAlex.
- CEP170 as a novel molecular link between centrosomal function and cerebral cortical development.Journal of biomedical science · 2026Article
- The βCirculation research · 2025Article
- Microtubules, Membranes, and Movement: New Roles for Stathmin-2 in Axon Integrity.Journal of neuroscience research · 2024Review
- Development of a 3-dimensional organotypic model with characteristics of peripheral sensory nerves.Cell reports methods · 2024Article
- Neurofilament Biophysics: From Structure to Biomechanics.Molecular biology of the cell · 2024Review
- Inactivity of Stat3 in sensory and non-sensory cells of the mature cochlea.Frontiers in molecular neuroscience · 2024Article
- Posttranscriptional regulation of neurofilament proteins and tau in health and disease.Brain research bulletin · 2023Review
- Neurofilaments in health and Charcot-Marie-Tooth disease.Frontiers in cell and developmental biology · 2023Review
- Editorial: Cytoskeletal alterations in aging and disease.Frontiers in cell and developmental biology · 2023Article
- Age-dependent increase of cytoskeletal components in sensory axons in human skin.Frontiers in cell and developmental biology · 2022Article
- Neurofilament Light Regulates Axon Caliber, Synaptic Activity, and Organelle Trafficking in Cultured Human Motor Neurons.Frontiers in cell and developmental biology · 2021Article
- Gaussian Embedding for Large-scale Gene Set Analysis.Nature machine intelligence · 2020Article
- Stathmin Regulates Spatiotemporal Variation in the Memory Loop in Single-Prolonged Stress Rats.Journal of molecular neuroscience : MN · 2020Article
- Absence of NEFL in patient-specific neurons in early-onset Charcot-Marie-Tooth neuropathy.Neurology. Genetics · 2018Article
- Neurobiology of axonal transport defects in motor neuron diseases: Opportunities for translational research?Neurobiology of disease · 2017Review
- A Case for Microtubule Vulnerability in Amyotrophic Lateral Sclerosis: Altered Dynamics During Disease.Frontiers in cellular neuroscience · 2016Review
- Article
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In neurons, microtubules form a dense array within axons, and the stability and function of this microtubule network is modulated by neurofilaments. Accumulation of neurofilaments has been observed in several forms of neurodegenerative diseases, but the mechanisms how elevated neurofilament levels destabilize axons are unknown so far. Here, we show that increased neurofilament expression in motor nerves of pmn mutant mice, a model of motoneuron disease, causes disturbed microtubule dynamics. The disease is caused by a point mutation in the tubulin-specific chaperone E (Tbce) gene, leading to an exchange of the most C-terminal amino acid tryptophan to glycine. As a consequence, the TBCE protein becomes instable which then results in destabilization of axonal microtubules and defects in axonal transport, in particular in motoneurons. Depletion of neurofilament increases the number and regrowth of microtubules in pmn mutant motoneurons and restores axon elongation. This effect is mediated by interaction of neurofilament with the stathmin complex. Accumulating neurofilaments associate with stathmin in axons of pmn mutant motoneurons. Depletion of neurofilament by Nefl knockout increases Stat3-stathmin interaction and stabilizes the microtubules in pmn mutant motoneurons. Consequently, counteracting enhanced neurofilament expression improves axonal maintenance and prolongs survival of pmn mutant mice. We propose that this mechanism could also be relevant for other neurodegenerative diseases in which neurofilament accumulation and loss of microtubules are prominent features.
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