α-synuclein strains that cause distinct pathologies differentially inhibit proteasome.


Journal

eLife
ISSN: 2050-084X
Titre abrégé: Elife
Pays: England
ID NLM: 101579614

Informations de publication

Date de publication:
22 07 2020
Historique:
received: 11 03 2020
accepted: 22 07 2020
pubmed: 23 7 2020
medline: 13 2 2021
entrez: 23 7 2020
Statut: epublish

Résumé

Abnormal α-synuclein aggregation has been implicated in several diseases and is known to spread in a prion-like manner. There is a relationship between protein aggregate structure (strain) and clinical phenotype in prion diseases, however, whether differences in the strains of α-synuclein aggregates account for the different pathologies remained unclear. Here, we generated two types of α-synuclein fibrils from identical monomer and investigated their seeding and propagation ability in mice and primary-cultured neurons. One α-synuclein fibril induced marked accumulation of phosphorylated α-synuclein and ubiquitinated protein aggregates, while the other did not, indicating the formation of α-synuclein two strains. Notably, the former α-synuclein strain inhibited proteasome activity and co-precipitated with 26S proteasome complex. Further examination indicated that structural differences in the C-terminal region of α-synuclein strains lead to different effects on proteasome activity. These results provide a possible molecular mechanism to account for the different pathologies induced by different α-synuclein strains.

Identifiants

pubmed: 32697196
doi: 10.7554/eLife.56825
pii: 56825
pmc: PMC7406352
doi:
pii:

Substances chimiques

Fungal Proteins 0
alpha-Synuclein 0
Proteasome Endopeptidase Complex EC 3.4.25.1
ATP dependent 26S protease EC 3.4.99.-

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Japan Society for the Promotion of Science
ID : 16K21650
Pays : International
Organisme : Ministry of Education, Culture, Sports, Science, and Technology
ID : 26117005
Pays : International
Organisme : Core Research for Evolutional Science and Technology
ID : JPMJCR18H3
Pays : International
Organisme : Japan Agency for Medical Research and Development
ID : JP18dm0207019
Pays : International

Informations de copyright

© 2020, Suzuki et al.

Déclaration de conflit d'intérêts

GS, SI, MH, RK, TN, SH, YS, MH No competing interests declared

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Auteurs

Genjiro Suzuki (G)

Dementia Research Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.

Sei Imura (S)

Dementia Research Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Laboratory of Molecular Neuroscience, Department of Biological Sciences, Tokyo Metropolitan University, Tokyo, Japan.

Masato Hosokawa (M)

Dementia Research Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.

Ryu Katsumata (R)

Dementia Research Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.

Takashi Nonaka (T)

Dementia Research Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.

Shin-Ichi Hisanaga (SI)

Laboratory of Molecular Neuroscience, Department of Biological Sciences, Tokyo Metropolitan University, Tokyo, Japan.

Yasushi Saeki (Y)

Protein Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.

Masato Hasegawa (M)

Dementia Research Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.

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Classifications MeSH