In the developing brain, the polarity of neural progenitor cells, termed radial glial cells (RGCs), is important for neurogenesis. Intercellular adhesions, termed apical junctional complexes (AJCs), at the apical surface between RGCs are necessary for cell polarization. However, the mechanism by which AJCs are established remains unclear. Here, we show that a SNARE complex composed of SNAP23, VAMP8, and Syntaxin1B has crucial roles in AJC formation and RGC polarization. Central nervous system (CNS)–specific ablation of SNAP23 (NcKO) results in mice with severe hypoplasia of the neocortex and no hippocampus or cerebellum. In the developing NcKO brain, RGCs lose their polarity following the disruption of AJCs and exhibit reduced proliferation, increased differentiation, and increased apoptosis. SNAP23 and its partner SNAREs, VAMP8 and Syntaxin1B, are important for the localization of an AJC protein, N-cadherin, to the apical plasma membrane of RGCs. Altogether, SNARE-mediated localization of N-cadherin is essential for AJC formation and RGC polarization during brain development.
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4 January 2021
Article|
December 17 2020
SNAP23 deficiency causes severe brain dysplasia through the loss of radial glial cell polarity
Masataka Kunii,
1
Department of Cell Biology, Graduate School of Medicine, Osaka University, Osaka, Japan
2
Laboratory of Molecular Traffic, Department of Molecular and Cellular Biology, Institute for Molecular and Cellular Regulation, Gunma University, Gunma, Japan
Masataka Kunii: mstk921@acb.med.osaka-u.ac.jp
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Yuria Noguchi,
Yuria Noguchi
1
Department of Cell Biology, Graduate School of Medicine, Osaka University, Osaka, Japan
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Shin-ichiro Yoshimura,
Shin-ichiro Yoshimura
1
Department of Cell Biology, Graduate School of Medicine, Osaka University, Osaka, Japan
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Satoshi Kanda,
Satoshi Kanda
1
Department of Cell Biology, Graduate School of Medicine, Osaka University, Osaka, Japan
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Tomohiko Iwano,
Tomohiko Iwano
3
Department of Anatomy and Cell Biology, Graduate School of Medicine, University of Yamanashi, Yamanashi, Japan
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Erda Avriyanti,
Erda Avriyanti
1
Department of Cell Biology, Graduate School of Medicine, Osaka University, Osaka, Japan
4
Department of Dermatology and Venereology, Faculty of Medicine, Padjadjaran University, Bandung, Indonesia
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Nur Atik,
Nur Atik
1
Department of Cell Biology, Graduate School of Medicine, Osaka University, Osaka, Japan
5
Department of Biomedical Sciences, Faculty of Medicine, Padjadjaran University, Bandung, Indonesia
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Takashi Sato,
Takashi Sato
6
Laboratory of Developmental Biology and Metabolism, Department of Molecular Medicine, Institute for Molecular and Cellular Regulation, Gunma University, Gunma, Japan
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Ken Sato,
Ken Sato
2
Laboratory of Molecular Traffic, Department of Molecular and Cellular Biology, Institute for Molecular and Cellular Regulation, Gunma University, Gunma, Japan
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Masaharu Ogawa,
Masaharu Ogawa
7
RIKEN Brain Science Institute, Saitama, Japan
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Akihiro Harada
1
Department of Cell Biology, Graduate School of Medicine, Osaka University, Osaka, Japan
2
Laboratory of Molecular Traffic, Department of Molecular and Cellular Biology, Institute for Molecular and Cellular Regulation, Gunma University, Gunma, Japan
Correspondence to Akihiro Harada: aharada@acb.med.osaka-u.ac.jp
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Masataka Kunii
1
Department of Cell Biology, Graduate School of Medicine, Osaka University, Osaka, Japan
2
Laboratory of Molecular Traffic, Department of Molecular and Cellular Biology, Institute for Molecular and Cellular Regulation, Gunma University, Gunma, Japan
Yuria Noguchi
1
Department of Cell Biology, Graduate School of Medicine, Osaka University, Osaka, Japan
Shin-ichiro Yoshimura
1
Department of Cell Biology, Graduate School of Medicine, Osaka University, Osaka, Japan
Satoshi Kanda
1
Department of Cell Biology, Graduate School of Medicine, Osaka University, Osaka, Japan
Tomohiko Iwano
3
Department of Anatomy and Cell Biology, Graduate School of Medicine, University of Yamanashi, Yamanashi, Japan
Erda Avriyanti
1
Department of Cell Biology, Graduate School of Medicine, Osaka University, Osaka, Japan
4
Department of Dermatology and Venereology, Faculty of Medicine, Padjadjaran University, Bandung, Indonesia
1
Department of Cell Biology, Graduate School of Medicine, Osaka University, Osaka, Japan
5
Department of Biomedical Sciences, Faculty of Medicine, Padjadjaran University, Bandung, Indonesia
Takashi Sato
6
Laboratory of Developmental Biology and Metabolism, Department of Molecular Medicine, Institute for Molecular and Cellular Regulation, Gunma University, Gunma, Japan
2
Laboratory of Molecular Traffic, Department of Molecular and Cellular Biology, Institute for Molecular and Cellular Regulation, Gunma University, Gunma, Japan
Masaharu Ogawa
7
RIKEN Brain Science Institute, Saitama, Japan
Akihiro Harada
1
Department of Cell Biology, Graduate School of Medicine, Osaka University, Osaka, Japan
2
Laboratory of Molecular Traffic, Department of Molecular and Cellular Biology, Institute for Molecular and Cellular Regulation, Gunma University, Gunma, Japan
Correspondence to Akihiro Harada: aharada@acb.med.osaka-u.ac.jp
Masataka Kunii: mstk921@acb.med.osaka-u.ac.jp
Received:
October 13 2019
Revision Received:
August 23 2020
Accepted:
October 23 2020
Online Issn: 1540-8140
Print Issn: 0021-9525
Funding:
Gunma University
(NO AWARD)
Japan Society for the Promotion of Science
(JP15H04668)
© 2020 Kunii et al.
2020
This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).
J Cell Biol (2021) 220 (1): e201910080.
Article history
Received:
October 13 2019
Revision Received:
August 23 2020
Accepted:
October 23 2020
Connected Content
Citation
Masataka Kunii, Yuria Noguchi, Shin-ichiro Yoshimura, Satoshi Kanda, Tomohiko Iwano, Erda Avriyanti, Nur Atik, Takashi Sato, Ken Sato, Masaharu Ogawa, Akihiro Harada; SNAP23 deficiency causes severe brain dysplasia through the loss of radial glial cell polarity. J Cell Biol 4 January 2021; 220 (1): e201910080. doi: https://doi.org/10.1083/jcb.201910080
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