Absence of ATG9A and synaptophysin demixing on Rab5 mutation-induced giant endosomes.
ATG9A
Endosomes
Liquid–liquid phase separation
Synaptophysin
Vesicle clusters
Journal
Molecular brain
ISSN: 1756-6606
Titre abrégé: Mol Brain
Pays: England
ID NLM: 101468876
Informations de publication
Date de publication:
02 Sep 2024
02 Sep 2024
Historique:
received:
29
03
2024
accepted:
07
08
2024
medline:
3
9
2024
pubmed:
3
9
2024
entrez:
2
9
2024
Statut:
epublish
Résumé
ATG9A is the only integral membrane protein among core autophagy-related (ATG) proteins. We previously found that ATG9A does not co-assemble into synaptophysin-positive vesicles, but rather, localizes to a distinct pool of vesicles within synapsin condensates in both fibroblasts and nerve terminals. The endocytic origin of these vesicles further suggests the existence of different intracellular sorting or segregation mechanisms for ATG9A and synaptophysin in cells. However, the precise underlying mechanism remains largely unknown. In this follow-up study, we investigated the endosomal localization of these two proteins by exploiting the advantages of a Rab5 mutant that induces the formation of enlarged endosomes. Notably, ATG9A and synaptophysin intermix perfectly and do not segregate on giant endosomes, indicating that the separation of these two proteins is not solely caused by the inherent properties of the proteins, but possibly by other unknown factors.
Identifiants
pubmed: 39223639
doi: 10.1186/s13041-024-01132-3
pii: 10.1186/s13041-024-01132-3
doi:
Substances chimiques
Synaptophysin
0
rab5 GTP-Binding Proteins
EC 3.6.5.2
Autophagy-Related Proteins
0
Membrane Proteins
0
Atg9A protein, mouse
0
Vesicular Transport Proteins
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
63Subventions
Organisme : The Catholic University of Korea
ID : 2023
Informations de copyright
© 2024. The Author(s).
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