Roles of Collagen XXV and Its Putative Receptors PTPσ/δ in Intramuscular Motor Innervation and Congenital Cranial Dysinnervation Disorder.


Journal

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

Informations de publication

Date de publication:
24 Dec 2019
Historique:
received: 15 03 2019
revised: 23 09 2019
accepted: 26 11 2019
entrez: 26 12 2019
pubmed: 26 12 2019
medline: 25 9 2020
Statut: ppublish

Résumé

Intramuscular motor innervation is an essential process in neuromuscular development. Recently, mutations in COL25A1, encoding CLAC-P/collagen XXV, have been linked to the development of a congenital cranial dysinnervation disorder (CCDD). Yet the molecular mechanisms of intramuscular innervation and the etiology of CCDD related to COL25A1 have remained elusive. Here, we report that muscle-derived collagen XXV is indispensable for intramuscular innervation. In developing skeletal muscles, Col25a1 expression is tightly regulated by muscle excitation. In vitro and cell-based assays reveal a direct interaction between collagen XXV and receptor protein tyrosine phosphatases (PTPs) σ and δ. Motor explant assays show that expression of collagen XXV in target cells attracts motor axons, but this is inhibited by exogenous PTPσ/δ. CCDD mutations attenuate motor axon attraction by reducing collagen XXV-PTPσ/δ interaction. Overall, our study identifies PTPσ/δ as putative receptors for collagen XXV, implicating collagen XXV and PTPσ/δ in intramuscular innervation and a developmental ocular motor disorder.

Identifiants

pubmed: 31875546
pii: S2211-1247(19)31635-3
doi: 10.1016/j.celrep.2019.11.112
pii:
doi:

Substances chimiques

Non-Fibrillar Collagens 0
Protein Tyrosine Phosphatases, Non-Receptor EC 3.1.3.48
Ptpn21 protein, mouse EC 3.1.3.48
Ptprs protein, mouse EC 3.1.3.48
Receptor-Like Protein Tyrosine Phosphatases, Class 2 EC 3.1.3.48

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

4362-4376.e6

Informations de copyright

Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.

Auteurs

Haruka Munezane (H)

Department of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.

Hiroaki Oizumi (H)

Department of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.

Tomoko Wakabayashi (T)

Department of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan; Department of Innovative Dementia Prevention, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan. Electronic address: tomoko-wakabayashi@umin.ac.jp.

Shu Nishio (S)

Department of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.

Tomoko Hirasawa (T)

Department of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.

Takashi Sato (T)

Laboratory of Developmental Biology and Metabolism, Institute for Molecular and Cellular Regulation, Gunma University, Gunma 371-8512, Japan.

Akihiro Harada (A)

Department of Cell Biology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.

Tomoyuki Yoshida (T)

Department of Molecular Neuroscience, University of Toyama, Toyama 930-0194, Japan.

Takahiro Eguchi (T)

Division of Genetics, Department of Cancer Biology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.

Yuji Yamanashi (Y)

Division of Genetics, Department of Cancer Biology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.

Tadafumi Hashimoto (T)

Department of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan; Department of Innovative Dementia Prevention, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.

Takeshi Iwatsubo (T)

Department of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan. Electronic address: iwatsubo@m.u-tokyo.ac.jp.

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Classifications MeSH