Tipping point in α-synuclein-membrane interactions from stable protein-covered vesicles to amyloid aggregation
(2024) In Cell Reports Physical Science 5(12).- Abstract
α-synuclein is a neuronal protein implicated in neurotransmitter release. Its function is thought to critically depend on the dynamic equilibrium between its free and its membrane-bound state. α-synuclein amyloid formation, implicated in Parkinson's disease, is also modulated by lipid membranes. The interplay between these processes remains elusive yet relates to the outstanding question of what determines the switch between physiological and disease-related behavior of the protein. Here, we study the coupling of equilibrium between free and membrane-bound α-synuclein and membrane-induced amyloid formation at lipid-to-protein ratios where amyloid formation is either accelerated or inhibited by lipid membranes. We find a clear difference... (More)
α-synuclein is a neuronal protein implicated in neurotransmitter release. Its function is thought to critically depend on the dynamic equilibrium between its free and its membrane-bound state. α-synuclein amyloid formation, implicated in Parkinson's disease, is also modulated by lipid membranes. The interplay between these processes remains elusive yet relates to the outstanding question of what determines the switch between physiological and disease-related behavior of the protein. Here, we study the coupling of equilibrium between free and membrane-bound α-synuclein and membrane-induced amyloid formation at lipid-to-protein ratios where amyloid formation is either accelerated or inhibited by lipid membranes. We find a clear difference between the exchange dynamics and the heterogeneity of the protein-covered membrane interface under these two sets of conditions. Our results highlight a strong coupling of membrane-modulated amyloid formation and the equilibrium between free and membrane-bound α-synuclein, which advances our molecular understanding of the physiological function of α-synuclein and its aberrant aggregation.
(Less)
- author
- Makasewicz, Katarzyna
LU
; Carlström, Göran
LU
; Stenström, Olof LU ; Bernfur, Katja LU ; Fridolf, Simon LU ; Akke, Mikael LU
; Linse, Sara LU and Sparr, Emma LU
- organization
-
- Physical Chemistry
- MultiPark: Multidisciplinary research focused on Parkinson´s disease
- LU Profile Area: Light and Materials
- Biophysical Chemistry
- Biochemistry and Structural Biology
- NanoLund: Centre for Nanoscience
- LTH Profile Area: Nanoscience and Semiconductor Technology
- LU Profile Area: Proactive Ageing
- publishing date
- 2024-12
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- amyloid formation, exchange dynamics, HSQC NMR, lipid membranes, PFG diffusion NMR, protein corona, protein-lipid co-aggregation, protein-membrane interactions, α-synuclein
- in
- Cell Reports Physical Science
- volume
- 5
- issue
- 12
- article number
- 102309
- publisher
- Cell Press
- external identifiers
-
- scopus:85212349235
- ISSN
- 2666-3864
- DOI
- 10.1016/j.xcrp.2024.102309
- language
- English
- LU publication?
- yes
- id
- 04ecfa70-b985-441a-a4b8-c34089551ca0
- date added to LUP
- 2025-01-20 11:11:53
- date last changed
- 2025-04-04 14:24:39
@article{04ecfa70-b985-441a-a4b8-c34089551ca0, abstract = {{<p>α-synuclein is a neuronal protein implicated in neurotransmitter release. Its function is thought to critically depend on the dynamic equilibrium between its free and its membrane-bound state. α-synuclein amyloid formation, implicated in Parkinson's disease, is also modulated by lipid membranes. The interplay between these processes remains elusive yet relates to the outstanding question of what determines the switch between physiological and disease-related behavior of the protein. Here, we study the coupling of equilibrium between free and membrane-bound α-synuclein and membrane-induced amyloid formation at lipid-to-protein ratios where amyloid formation is either accelerated or inhibited by lipid membranes. We find a clear difference between the exchange dynamics and the heterogeneity of the protein-covered membrane interface under these two sets of conditions. Our results highlight a strong coupling of membrane-modulated amyloid formation and the equilibrium between free and membrane-bound α-synuclein, which advances our molecular understanding of the physiological function of α-synuclein and its aberrant aggregation.</p>}}, author = {{Makasewicz, Katarzyna and Carlström, Göran and Stenström, Olof and Bernfur, Katja and Fridolf, Simon and Akke, Mikael and Linse, Sara and Sparr, Emma}}, issn = {{2666-3864}}, keywords = {{amyloid formation; exchange dynamics; HSQC NMR; lipid membranes; PFG diffusion NMR; protein corona; protein-lipid co-aggregation; protein-membrane interactions; α-synuclein}}, language = {{eng}}, number = {{12}}, publisher = {{Cell Press}}, series = {{Cell Reports Physical Science}}, title = {{Tipping point in α-synuclein-membrane interactions from stable protein-covered vesicles to amyloid aggregation}}, url = {{http://dx.doi.org/10.1016/j.xcrp.2024.102309}}, doi = {{10.1016/j.xcrp.2024.102309}}, volume = {{5}}, year = {{2024}}, }