The cellular architecture and molecular determinants of the zebrafish fusogenic synapse.

Jam2a/Jamb Jam3b/Jamc Myomaker Myomixer WASP and WAVE actin cytoskeleton cell-cell fusion invasive membrane protrusions myoblast fusion zebrafish muscle development

Journal

Developmental cell
ISSN: 1878-1551
Titre abrégé: Dev Cell
Pays: United States
ID NLM: 101120028

Informations de publication

Date de publication:
11 07 2022
Historique:
received: 08 09 2021
revised: 04 04 2022
accepted: 20 05 2022
pubmed: 17 6 2022
medline: 15 7 2022
entrez: 16 6 2022
Statut: ppublish

Résumé

Myoblast fusion is an indispensable process in skeletal muscle development and regeneration. Studies in Drosophila led to the discovery of the asymmetric fusogenic synapse, in which one cell invades its fusion partner with actin-propelled membrane protrusions to promote fusion. However, the timing and sites of vertebrate myoblast fusion remain elusive. Here, we show that fusion between zebrafish fast muscle cells is mediated by an F-actin-enriched invasive structure. Two cell adhesion molecules, Jam2a and Jam3b, are associated with the actin structure, with Jam2a being the major organizer. The Arp2/3 actin nucleation-promoting factors, WAVE and WASP-but not the bipartite fusogenic proteins, Myomaker or Myomixer-promote the formation of the invasive structure. Moreover, the convergence of fusogen-containing microdomains and the invasive protrusions is a prerequisite for cell membrane fusion. Thus, our study provides unprecedented insights into the cellular architecture and molecular determinants of the asymmetric fusogenic synapse in an intact vertebrate animal.

Identifiants

pubmed: 35709765
pii: S1534-5807(22)00373-2
doi: 10.1016/j.devcel.2022.05.016
pmc: PMC10180866
mid: NIHMS1811041
pii:
doi:

Substances chimiques

Actins 0
Membrane Proteins 0
Muscle Proteins 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

1582-1597.e6

Subventions

Organisme : NIAMS NIH HHS
ID : R01 AR053173
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR075005
Pays : United States
Organisme : NIGMS NIH HHS
ID : R35 GM136316
Pays : United States
Organisme : NIH HHS
ID : S10 OD021685
Pays : United States

Informations de copyright

Copyright © 2022 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests The authors declare no competing interests.

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Auteurs

Zhou Luo (Z)

Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.

Jun Shi (J)

Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address: jun.shi@utsouthwestern.edu.

Pratima Pandey (P)

Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.

Zhi-Rong Ruan (ZR)

Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.

Maria Sevdali (M)

Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

Ye Bu (Y)

Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

Yue Lu (Y)

Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.

Shaojun Du (S)

Institute of Marine and Environmental Technology, Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD, USA.

Elizabeth H Chen (EH)

Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA; Department of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA; Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA; Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address: elizabeth.chen@utsouthwestern.edu.

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