Dynamin-2 Regulates Postsynaptic Cytoskeleton Organization and Neuromuscular Junction Development.

NMJ morphogenesis actin-bundling protein centronuclear myopathy phosphorylation of Dyn2(Y597) podosome turnover postsynaptic actin

Journal

Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691

Informations de publication

Date de publication:
27 10 2020
Historique:
received: 03 03 2020
revised: 23 09 2020
accepted: 05 10 2020
entrez: 28 10 2020
pubmed: 29 10 2020
medline: 20 11 2021
Statut: ppublish

Résumé

Neuromuscular junctions (NMJs) govern efficient neuronal communication with muscle cells, relying on proper architecture of specialized postsynaptic compartments. However, the intrinsic mechanism in muscle cells contributing to NMJ development remains unclear. In this study, we reveal that dynamin-2 (Dyn2) is involved in postsynaptic development of NMJs. Mutations of Dyn2 have been linked to human muscular disorder and centronuclear myopathy (CNM), as well as featured with muscle atrophy and defective NMJs, yet the function of Dyn2 at the postsynaptic membrane is largely unknown. We demonstrate that Dyn2 is enriched at the postsynaptic membrane and regulates NMJ development via actin remodeling. Dyn2 functions as an actin-bundling GTPase to regulate podosome turnover and cytoskeletal organization of the postsynaptic apparatus, and CNM-Dyn2 mutations display abnormal actin remodeling and electrophysiological activity of fly NMJs. Altogether, Dyn2 primarily regulates actin cytoskeleton remodeling and NMJ morphogenesis at the postsynaptic membrane, which is distinct from its endocytosis regulatory role at the presynaptic membrane.

Identifiants

pubmed: 33113375
pii: S2211-1247(20)31299-7
doi: 10.1016/j.celrep.2020.108310
pii:
doi:

Substances chimiques

DNM2 protein, human EC 3.6.5.5
Dynamin II EC 3.6.5.5

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

108310

Informations de copyright

Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Interests The authors declare no competing interests.

Auteurs

Shan-Shan Lin (SS)

Institute of Molecular Medicine, College of Medicine, National Taiwan University, Taipei 100, Taiwan.

Tsung-Lin Hsieh (TL)

Institute of Molecular Medicine, College of Medicine, National Taiwan University, Taipei 100, Taiwan.

Gunn-Guang Liou (GG)

Institute of Biological Chemistry, Academia Sinica, Taipei 115, Taiwan.

Tsai-Ning Li (TN)

Institute of Biological Chemistry, Academia Sinica, Taipei 115, Taiwan.

Hsin-Chieh Lin (HC)

Institute of Biological Chemistry, Academia Sinica, Taipei 115, Taiwan.

Chiung-Wen Chang (CW)

Institute of Biological Chemistry, Academia Sinica, Taipei 115, Taiwan.

Hsiang-Yi Wu (HY)

Institute of Biological Chemistry, Academia Sinica, Taipei 115, Taiwan.

Chi-Kuang Yao (CK)

Institute of Biological Chemistry, Academia Sinica, Taipei 115, Taiwan.

Ya-Wen Liu (YW)

Institute of Molecular Medicine, College of Medicine, National Taiwan University, Taipei 100, Taiwan; Center of Precision Medicine, College of Medicine, National Taiwan University, Taipei 100, Taiwan. Electronic address: yawenliu@ntu.edu.tw.

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Classifications MeSH