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The vesicular SNARE Synaptobrevin is required for Semaphorin 3A axonal repulsion
Attractive and repulsive molecules such as Semaphorins (Sema) trigger rapid responses that control the navigation of axonal growth cones. The role of vesicular traffic in axonal guidance is still largely unknown. The exocytic vesicular soluble N-ethylmaleimide sensitive fusion protein attachment pro...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3255983/ https://www.ncbi.nlm.nih.gov/pubmed/22213797 http://dx.doi.org/10.1083/jcb.201106113 |
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author | Zylbersztejn, Kathleen Petkovic, Maja Burgo, Andrea Deck, Marie Garel, Sonia Marcos, Séverine Bloch-Gallego, Evelyne Nothias, Fatiha Serini, Guido Bagnard, Dominique Binz, Thomas Galli, Thierry |
author_facet | Zylbersztejn, Kathleen Petkovic, Maja Burgo, Andrea Deck, Marie Garel, Sonia Marcos, Séverine Bloch-Gallego, Evelyne Nothias, Fatiha Serini, Guido Bagnard, Dominique Binz, Thomas Galli, Thierry |
author_sort | Zylbersztejn, Kathleen |
collection | PubMed |
description | Attractive and repulsive molecules such as Semaphorins (Sema) trigger rapid responses that control the navigation of axonal growth cones. The role of vesicular traffic in axonal guidance is still largely unknown. The exocytic vesicular soluble N-ethylmaleimide sensitive fusion protein attachment protein receptor (SNARE) Synaptobrevin 2 (Syb2) is known for mediating neurotransmitter release in mature neurons, but its potential role in axonal guidance remains elusive. Here we show that Syb2 is required for Sema3A-dependent repulsion but not Sema3C-dependent attraction in cultured neurons and in the mouse brain. Syb2 associated with Neuropilin 1 and Plexin A1, two essential components of the Sema3A receptor, via its juxtatransmembrane domain. Sema3A receptor and Syb2 colocalize in endosomal membranes. Moreover, upon Sema3A treatment, Syb2-deficient neurons failed to collapse and transport Plexin A1 to cell bodies. Reconstitution of Sema3A receptor in nonneuronal cells revealed that Sema3A further inhibited the exocytosis of Syb2. Therefore, Sema3A-mediated signaling and axonal repulsion require Syb2-dependent vesicular traffic. |
format | Online Article Text |
id | pubmed-3255983 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-32559832012-07-09 The vesicular SNARE Synaptobrevin is required for Semaphorin 3A axonal repulsion Zylbersztejn, Kathleen Petkovic, Maja Burgo, Andrea Deck, Marie Garel, Sonia Marcos, Séverine Bloch-Gallego, Evelyne Nothias, Fatiha Serini, Guido Bagnard, Dominique Binz, Thomas Galli, Thierry J Cell Biol Research Articles Attractive and repulsive molecules such as Semaphorins (Sema) trigger rapid responses that control the navigation of axonal growth cones. The role of vesicular traffic in axonal guidance is still largely unknown. The exocytic vesicular soluble N-ethylmaleimide sensitive fusion protein attachment protein receptor (SNARE) Synaptobrevin 2 (Syb2) is known for mediating neurotransmitter release in mature neurons, but its potential role in axonal guidance remains elusive. Here we show that Syb2 is required for Sema3A-dependent repulsion but not Sema3C-dependent attraction in cultured neurons and in the mouse brain. Syb2 associated with Neuropilin 1 and Plexin A1, two essential components of the Sema3A receptor, via its juxtatransmembrane domain. Sema3A receptor and Syb2 colocalize in endosomal membranes. Moreover, upon Sema3A treatment, Syb2-deficient neurons failed to collapse and transport Plexin A1 to cell bodies. Reconstitution of Sema3A receptor in nonneuronal cells revealed that Sema3A further inhibited the exocytosis of Syb2. Therefore, Sema3A-mediated signaling and axonal repulsion require Syb2-dependent vesicular traffic. The Rockefeller University Press 2012-01-09 /pmc/articles/PMC3255983/ /pubmed/22213797 http://dx.doi.org/10.1083/jcb.201106113 Text en © 2012 Zylbersztejn et al. 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 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/). |
spellingShingle | Research Articles Zylbersztejn, Kathleen Petkovic, Maja Burgo, Andrea Deck, Marie Garel, Sonia Marcos, Séverine Bloch-Gallego, Evelyne Nothias, Fatiha Serini, Guido Bagnard, Dominique Binz, Thomas Galli, Thierry The vesicular SNARE Synaptobrevin is required for Semaphorin 3A axonal repulsion |
title | The vesicular SNARE Synaptobrevin is required for Semaphorin 3A axonal repulsion |
title_full | The vesicular SNARE Synaptobrevin is required for Semaphorin 3A axonal repulsion |
title_fullStr | The vesicular SNARE Synaptobrevin is required for Semaphorin 3A axonal repulsion |
title_full_unstemmed | The vesicular SNARE Synaptobrevin is required for Semaphorin 3A axonal repulsion |
title_short | The vesicular SNARE Synaptobrevin is required for Semaphorin 3A axonal repulsion |
title_sort | vesicular snare synaptobrevin is required for semaphorin 3a axonal repulsion |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3255983/ https://www.ncbi.nlm.nih.gov/pubmed/22213797 http://dx.doi.org/10.1083/jcb.201106113 |
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