Home > Publications Database > Synapsin Condensates Recruit alpha-Synuclein. > print

001     154773
005     20230915092313.0
024 7 _ |a 10.1016/j.jmb.2021.166961
|2 doi
024 7 _ |a pmid:33774037
|2 pmid
024 7 _ |a 0022-2836
|2 ISSN
024 7 _ |a 1089-8638
|2 ISSN
024 7 _ |a altmetric:103000811
|2 altmetric
037 _ _ |a DZNE-2021-00363
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Hoffmann, Christian
|0 P:(DE-2719)9000582
|b 0
|e First author
245 _ _ |a Synapsin Condensates Recruit alpha-Synuclein.
260 _ _ |a Amsterdam [u.a.]
|c 2021
|b Elsevier
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1683797294_30877
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a Neurotransmission relies on the tight spatial and temporal regulation of the synaptic vesicle (SV) cycle. Nerve terminals contain hundreds of SVs that form tight clusters. These clusters represent a distinct liquid phase in which one component of the phase are SVs and the other synapsin 1, a highly abundant synaptic protein. Another major family of disordered proteins at the presynapse includes synucleins, most notably α-synuclein. The precise physiological role of α-synuclein in synaptic physiology remains elusive, albeit its role has been implicated in nearly all steps of the SV cycle. To determine the effect of α-synuclein on the synapsin phase, we employ the reconstitution approach using natively purified SVs from rat brains and the heterologous cell system to generate synapsin condensates. We demonstrate that synapsin condensates recruit α-synuclein, and while enriched into these synapsin condensates, α-synuclein still maintains its high mobility. The presence of SVs enhances the rate of synapsin/α-synuclein condensation, suggesting that SVs act as catalyzers for the formation of synapsin condensates. Notably, at physiological salt and protein concentrations, α-synuclein alone is not able to cluster isolated SVs. Excess of α-synuclein disrupts the kinetics of synapsin/SV condensate formation, indicating that the molar ratio between synapsin and α-synuclein is important in assembling the functional condensates of SVs. Understanding the molecular mechanism of α-synuclein interactions at the nerve terminals is crucial for clarifying the pathogenesis of synucleinopathies, where α-synuclein, synaptic proteins and lipid organelles all accumulate as insoluble intracellular inclusions.
536 _ _ |a 351 - Brain Function (POF4-351)
|0 G:(DE-HGF)POF4-351
|c POF4-351
|f POF IV
|x 0
536 _ _ |a 352 - Disease Mechanisms (POF4-352)
|0 G:(DE-HGF)POF4-352
|c POF4-352
|f POF IV
|x 1
588 _ _ |a Dataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
650 _ 7 |a liquid-liquid phase separation
|2 Other
650 _ 7 |a synapsin 1
|2 Other
650 _ 7 |a synaptic vesicles
|2 Other
650 _ 7 |a synucleinopathies
|2 Other
650 _ 7 |a α-synuclein
|2 Other
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Brain: cytology
|2 MeSH
650 _ 2 |a Brain: metabolism
|2 MeSH
650 _ 2 |a HEK293 Cells
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Luminescent Proteins: genetics
|2 MeSH
650 _ 2 |a Luminescent Proteins: metabolism
|2 MeSH
650 _ 2 |a Macromolecular Substances: chemistry
|2 MeSH
650 _ 2 |a Macromolecular Substances: metabolism
|2 MeSH
650 _ 2 |a Microscopy, Confocal
|2 MeSH
650 _ 2 |a Microscopy, Fluorescence
|2 MeSH
650 _ 2 |a Rats
|2 MeSH
650 _ 2 |a Synapsins: chemistry
|2 MeSH
650 _ 2 |a Synapsins: metabolism
|2 MeSH
650 _ 2 |a Synaptic Transmission
|2 MeSH
650 _ 2 |a Synaptic Vesicles: metabolism
|2 MeSH
650 _ 2 |a alpha-Synuclein: chemistry
|2 MeSH
650 _ 2 |a alpha-Synuclein: metabolism
|2 MeSH
700 1 _ |a Sansevrino, Roberto
|0 P:(DE-2719)9000736
|b 1
|e First author
700 1 _ |a Morabito, Giuseppe
|0 P:(DE-2719)9001233
|b 2
700 1 _ |a Logan, Chinyere
|0 P:(DE-2719)9001041
|b 3
700 1 _ |a Vabulas, R Martin
|0 P:(DE-HGF)0
|b 4
700 1 _ |a Ulusoy, Ayse
|0 P:(DE-2719)2772760
|b 5
700 1 _ |a Ganzella, Marcelo
|0 P:(DE-HGF)0
|b 6
700 1 _ |a Milovanovic, Dragomir
|0 P:(DE-2719)9000670
|b 7
|e Last author
773 _ _ |a 10.1016/j.jmb.2021.166961
|g Vol. 433, no. 12, p. 166961 -
|0 PERI:(DE-600)1355192-9
|n 12
|p 166961
|t Journal of molecular biology
|v 433
|y 2021
|x 0022-2836
856 4 _ |u https://www.sciencedirect.com/science/article/pii/S0022283621001625
856 4 _ |u https://pub.dzne.de/record/154773/files/DZNE-2021-00363.pdf
|y OpenAccess
856 4 _ |u https://pub.dzne.de/record/154773/files/DZNE-2021-00363.pdf?subformat=pdfa
|x pdfa
|y OpenAccess
909 C O |o oai:pub.dzne.de:154773
|p openaire
|p open_access
|p VDB
|p driver
|p dnbdelivery
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 0
|6 P:(DE-2719)9000582
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 1
|6 P:(DE-2719)9000736
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 2
|6 P:(DE-2719)9001233
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 3
|6 P:(DE-2719)9001041
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 5
|6 P:(DE-2719)2772760
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 7
|6 P:(DE-2719)9000670
913 1 _ |a DE-HGF
|b Gesundheit
|l Neurodegenerative Diseases
|1 G:(DE-HGF)POF4-350
|0 G:(DE-HGF)POF4-351
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Brain Function
|x 0
913 1 _ |a DE-HGF
|b Gesundheit
|l Neurodegenerative Diseases
|1 G:(DE-HGF)POF4-350
|0 G:(DE-HGF)POF4-352
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Disease Mechanisms
|x 1
913 0 _ |a DE-HGF
|b Gesundheit
|l Erkrankungen des Nervensystems
|1 G:(DE-HGF)POF3-340
|0 G:(DE-HGF)POF3-342
|3 G:(DE-HGF)POF3
|2 G:(DE-HGF)POF3-300
|4 G:(DE-HGF)POF
|v Disease Mechanisms and Model Systems
|x 0
914 1 _ |y 2021
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1190
|2 StatID
|b Biological Abstracts
|d 2021-02-03
915 _ _ |a WoS
|0 StatID:(DE-HGF)0113
|2 StatID
|b Science Citation Index Expanded
|d 2021-02-03
915 _ _ |a OpenAccess
|0 StatID:(DE-HGF)0510
|2 StatID
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0160
|2 StatID
|b Essential Science Indicators
|d 2021-02-03
915 _ _ |a Creative Commons Attribution CC BY 4.0
|0 LIC:(DE-HGF)CCBY4
|2 HGFVOC
915 _ _ |a Nationallizenz
|0 StatID:(DE-HGF)0420
|2 StatID
|d 2022-11-08
|w ger
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b J MOL BIOL : 2021
|d 2022-11-08
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
|d 2022-11-08
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
|d 2022-11-08
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0600
|2 StatID
|b Ebsco Academic Search
|d 2022-11-08
915 _ _ |a Peer Review
|0 StatID:(DE-HGF)0030
|2 StatID
|b ASC
|d 2022-11-08
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Clarivate Analytics Master Journal List
|d 2022-11-08
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
|d 2022-11-08
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1050
|2 StatID
|b BIOSIS Previews
|d 2022-11-08
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1030
|2 StatID
|b Current Contents - Life Sciences
|d 2022-11-08
915 _ _ |a IF >= 5
|0 StatID:(DE-HGF)9905
|2 StatID
|b J MOL BIOL : 2021
|d 2022-11-08
920 _ _ |l yes
920 1 _ |0 I:(DE-2719)1813002
|k AG Milovanovic ; AG Milovanovic
|l Molecular Neurobiology
|x 0
920 1 _ |0 I:(DE-2719)1013008
|k AG Di Monte
|l Neurodegeneration and Neuroprotection in Parkinson´s Disease
|x 1
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a UNRESTRICTED
980 _ _ |a I:(DE-2719)1813002
980 _ _ |a I:(DE-2719)1013008
980 1 _ |a FullTexts

LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21