Lipid packing defects are necessary and sufficient for membrane binding of α-synuclein

Abstract α-Synuclein (αSyn), an intrinsically disordered protein implicated in Parkinson’s disease, is thought to initiate aggregation by binding to cellular membranes. Previous studies suggest that anionic lipids are necessary for this binding. However, these studies largely focused on unmodified α...

Full description

Saved in:
Bibliographic Details
Main Authors: David H. Johnson, Orianna H. Kou, John M. White, Stephanie Y. Ramirez, Antonis Margaritakis, Peter J. Chung, Vance W. Jaeger, Wade F. Zeno
Format: Article
Language:English
Published: Nature Portfolio 2025-08-01
Series:Communications Biology
Online Access:https://doi.org/10.1038/s42003-025-08622-7
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849761477836144640
author David H. Johnson
Orianna H. Kou
John M. White
Stephanie Y. Ramirez
Antonis Margaritakis
Peter J. Chung
Vance W. Jaeger
Wade F. Zeno
author_facet David H. Johnson
Orianna H. Kou
John M. White
Stephanie Y. Ramirez
Antonis Margaritakis
Peter J. Chung
Vance W. Jaeger
Wade F. Zeno
author_sort David H. Johnson
collection DOAJ
description Abstract α-Synuclein (αSyn), an intrinsically disordered protein implicated in Parkinson’s disease, is thought to initiate aggregation by binding to cellular membranes. Previous studies suggest that anionic lipids are necessary for this binding. However, these studies largely focused on unmodified αSyn, while physiological αSyn is N-terminally acetylated (NTA). Our work challenges the long-standing paradigm that anionic lipids are necessary for αSyn binding by demonstrating that NTA diminishes αSyn’s reliance on anionic membranes, revealing that membrane packing defects (i.e., interfacial hydrophobicity) alone can drive membrane binding. Using fluorescence microscopy and circular dichroism spectroscopy, we monitored the binding of NTA-αSyn to membrane vesicles with different lipid compositions. Phosphatidylcholine and phosphatidylserine concentrations were varied to control surface charge, while phospholipid tail unsaturation and methylation were varied to modulate lipid packing. We also formulated cholesterol-containing membranes that mimicked the lipid composition of synaptic vesicles. In these membranes, all-atom molecular dynamics simulations were used to visualize and quantify membrane packing defects. Our results demonstrate that membrane packing defects are necessary for NTA-αSyn binding and that defect-rich membranes are sufficient for NTA-αSyn binding regardless of membrane charge. These findings provide a molecular mechanism by which lipid structural properties, such as poly-unsaturation, can regulate αSyn binding to physiological membranes.
format Article
id doaj-art-8efe2fdda1e84f7b93abcfe1fda43a67
institution DOAJ
issn 2399-3642
language English
publishDate 2025-08-01
publisher Nature Portfolio
record_format Article
series Communications Biology
spelling doaj-art-8efe2fdda1e84f7b93abcfe1fda43a672025-08-20T03:06:01ZengNature PortfolioCommunications Biology2399-36422025-08-018111510.1038/s42003-025-08622-7Lipid packing defects are necessary and sufficient for membrane binding of α-synucleinDavid H. Johnson0Orianna H. Kou1John M. White2Stephanie Y. Ramirez3Antonis Margaritakis4Peter J. Chung5Vance W. Jaeger6Wade F. Zeno7Mork Family Department of Chemical Engineering and Materials Science, University of Southern CaliforniaDepartment of Physics and Astronomy, University of Southern CaliforniaDepartment of Chemical Engineering, University of LouisvilleDepartment of Biological Sciences, University of Southern CaliforniaDepartment of Physics and Astronomy, University of Southern CaliforniaDepartment of Physics and Astronomy, University of Southern CaliforniaDepartment of Chemical Engineering, University of LouisvilleMork Family Department of Chemical Engineering and Materials Science, University of Southern CaliforniaAbstract α-Synuclein (αSyn), an intrinsically disordered protein implicated in Parkinson’s disease, is thought to initiate aggregation by binding to cellular membranes. Previous studies suggest that anionic lipids are necessary for this binding. However, these studies largely focused on unmodified αSyn, while physiological αSyn is N-terminally acetylated (NTA). Our work challenges the long-standing paradigm that anionic lipids are necessary for αSyn binding by demonstrating that NTA diminishes αSyn’s reliance on anionic membranes, revealing that membrane packing defects (i.e., interfacial hydrophobicity) alone can drive membrane binding. Using fluorescence microscopy and circular dichroism spectroscopy, we monitored the binding of NTA-αSyn to membrane vesicles with different lipid compositions. Phosphatidylcholine and phosphatidylserine concentrations were varied to control surface charge, while phospholipid tail unsaturation and methylation were varied to modulate lipid packing. We also formulated cholesterol-containing membranes that mimicked the lipid composition of synaptic vesicles. In these membranes, all-atom molecular dynamics simulations were used to visualize and quantify membrane packing defects. Our results demonstrate that membrane packing defects are necessary for NTA-αSyn binding and that defect-rich membranes are sufficient for NTA-αSyn binding regardless of membrane charge. These findings provide a molecular mechanism by which lipid structural properties, such as poly-unsaturation, can regulate αSyn binding to physiological membranes.https://doi.org/10.1038/s42003-025-08622-7
spellingShingle David H. Johnson
Orianna H. Kou
John M. White
Stephanie Y. Ramirez
Antonis Margaritakis
Peter J. Chung
Vance W. Jaeger
Wade F. Zeno
Lipid packing defects are necessary and sufficient for membrane binding of α-synuclein
Communications Biology
title Lipid packing defects are necessary and sufficient for membrane binding of α-synuclein
title_full Lipid packing defects are necessary and sufficient for membrane binding of α-synuclein
title_fullStr Lipid packing defects are necessary and sufficient for membrane binding of α-synuclein
title_full_unstemmed Lipid packing defects are necessary and sufficient for membrane binding of α-synuclein
title_short Lipid packing defects are necessary and sufficient for membrane binding of α-synuclein
title_sort lipid packing defects are necessary and sufficient for membrane binding of α synuclein
url https://doi.org/10.1038/s42003-025-08622-7
work_keys_str_mv AT davidhjohnson lipidpackingdefectsarenecessaryandsufficientformembranebindingofasynuclein
AT oriannahkou lipidpackingdefectsarenecessaryandsufficientformembranebindingofasynuclein
AT johnmwhite lipidpackingdefectsarenecessaryandsufficientformembranebindingofasynuclein
AT stephanieyramirez lipidpackingdefectsarenecessaryandsufficientformembranebindingofasynuclein
AT antonismargaritakis lipidpackingdefectsarenecessaryandsufficientformembranebindingofasynuclein
AT peterjchung lipidpackingdefectsarenecessaryandsufficientformembranebindingofasynuclein
AT vancewjaeger lipidpackingdefectsarenecessaryandsufficientformembranebindingofasynuclein
AT wadefzeno lipidpackingdefectsarenecessaryandsufficientformembranebindingofasynuclein