ArticleCell death & disease2024
Actin-nucleation promoting factor N-WASP influences alpha-synuclein condensates and pathology.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Neurotoxicity, α-synuclein pathology, and mitochondrial dysfunction: A comparative study of different mouse models of Parkinson's disease.Neural regeneration research · 2026Article
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- Mitochondrial Fission and Fusion Disorders and Autophagy Abnormalities in Parkinson's Disease.Neurochemical research · 2026Review
- Reversibility and β-sheet formation are decoupled in tau condensate aging.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Drug screening for α-synuclein aggregation inhibitors via multimodal graph neural network.Briefings in bioinformatics · 2026Article
- The synaptic vesicle cluster as a controller of pre- and postsynaptic structure and function.The Journal of physiology · 2025Review
- Article
- Condensates of synaptic vesicles and synapsin-1 mediate actin sequestering and polymerization.The EMBO journal · 2025Article
- Live-cell quantification reveals viscoelastic regulation of synapsin condensates by α-synuclein.Science advances · 2025Article
- Synapsin Condensation is Governed by Sequence-Encoded Molecular Grammars.Journal of molecular biology · 2025Article
- Condensates of synaptic vesicles and synapsin are molecular beacons for actin sequestering and polymerization.bioRxiv : the preprint server for biology · 2025Article
- The CCT chaperonin and actin modulate the ER and RNA-binding protein condensation during oogenesis and maintain translational repression of maternal mRNA and oocyte quality.Molecular biology of the cell · 2024Article
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Authors and funding
19 authors at 4 institutions in 3 countries.
Funding
Abstract
Abnormal intraneuronal accumulation of soluble and insoluble α-synuclein (α-Syn) is one of the main pathological hallmarks of synucleinopathies, such as Parkinson's disease (PD). It has been well documented that the reversible liquid-liquid phase separation of α-Syn can modulate synaptic vesicle condensates at the presynaptic terminals. However, α-Syn can also form liquid-like droplets that may convert into amyloid-enriched hydrogels or fibrillar polymorphs under stressful conditions. To advance our understanding on the mechanisms underlying α-Syn phase transition, we employed a series of unbiased proteomic analyses and found that actin and actin regulators are part of the α-Syn interactome. We focused on Neural Wiskott-Aldrich syndrome protein (N-WASP) because of its association with a rare early-onset familial form of PD. In cultured cells, we demonstrate that N-WASP undergoes phase separation and can be recruited to synapsin 1 liquid-like droplets, whereas it is excluded from α-Syn/synapsin 1 condensates. Consistently, we provide evidence that wsp-1/WASL loss of function alters the number and dynamics of α-Syn inclusions in the nematode Caenorhabditis elegans. Together, our findings indicate that N-WASP expression may create permissive conditions that promote α-Syn condensates and their potentially deleterious conversion into toxic species.
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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 Socratic graph.