ArticleScientific reports2020
Cofilin dysregulation alters actin turnover in frataxin-deficient neurons.
Article in Scientific reports, 2020. 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, 14 citations in OpenAlex.
- Friedreich ataxia transcriptomic dysregulation and identification of cell type-specific biomarkers: A systematic review and meta-analysis.bioRxiv : the preprint server for biology · 2026Article
- Article
- Coro1B and Coro1C regulate lamellipodia dynamics and cell motility by tuning branched actin turnover.The Journal of cell biology · 2022Article
- Frataxin Deficit Leads to Reduced Dynamics of Growth Cones in Dorsal Root Ganglia Neurons of Friedreich's Ataxia YG8sR Model: A Multilinear Algebra Approach.Frontiers in molecular neuroscience · 2022Article
- Review
- Cofilin and Neurodegeneration: New Functions for an Old but Gold Protein.Brain sciences · 2021Review
- Quantitative Proteomic Analysis of Primitive Neural Stem Cells from LRRK2 G2019S-Associated Parkinson's Disease Patient-Derived iPSCs.Life (Basel, Switzerland) · 2020Article
- Antioxidant Therapies and Oxidative Stress in Friedreich´s Ataxia: The Right Path or Just a Diversion?Antioxidants (Basel, Switzerland) · 2020Review
- Hereditary Ataxia: A Focus on Heme Metabolism and Fe-S Cluster Biogenesis.International journal of molecular sciences · 2020Review
- Actin Remodeling Defects Leading to Autoinflammation and Immune Dysregulation.Frontiers in immunology · 2020Review
- Ofloxacin as a Disruptor of Actin Aggresome "Hirano Bodies": A Potential Repurposed Drug for the Treatment of Neurodegenerative Diseases.Frontiers in aging neuroscience · 2020Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormalities in actin cytoskeleton have been linked to Friedreich's ataxia (FRDA), an inherited peripheral neuropathy characterised by an early loss of neurons in dorsal root ganglia (DRG) among other clinical symptoms. Despite all efforts to date, we still do not fully understand the molecular events that contribute to the lack of sensory neurons in FRDA. We studied the adult neuronal growth cone (GC) at the cellular and molecular level to decipher the connection between frataxin and actin cytoskeleton in DRG neurons of the well-characterised YG8R Friedreich's ataxia mouse model. Immunofluorescence studies in primary cultures of DRG from YG8R mice showed neurons with fewer and smaller GCs than controls, associated with an inhibition of neurite growth. In frataxin-deficient neurons, we also observed an increase in the filamentous (F)-actin/monomeric (G)-actin ratio (F/G-actin ratio) in axons and GCs linked to dysregulation of two crucial modulators of filamentous actin turnover, cofilin-1 and the actin-related protein (ARP) 2/3 complex. We show how the activation of cofilin is due to the increase in chronophin (CIN), a cofilin-activating phosphatase. Thus cofilin emerges, for the first time, as a link between frataxin deficiency and actin cytoskeleton alterations.
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