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Netrin1/DCC signaling promotes neuronal migration in the dorsal spinal cord

BACKGROUND: Newborn neurons often migrate before undergoing final differentiation, extending neurites, and forming synaptic connections. Therefore, neuronal migration is crucial for establishing neural circuitry during development. In the developing spinal cord, neuroprogenitors first undergo radial...

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Autores principales: Junge, Harald J., Yung, Andrea R., Goodrich, Lisa V., Chen, Zhe
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5081974/
https://www.ncbi.nlm.nih.gov/pubmed/27784329
http://dx.doi.org/10.1186/s13064-016-0074-x
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author Junge, Harald J.
Yung, Andrea R.
Goodrich, Lisa V.
Chen, Zhe
author_facet Junge, Harald J.
Yung, Andrea R.
Goodrich, Lisa V.
Chen, Zhe
author_sort Junge, Harald J.
collection PubMed
description BACKGROUND: Newborn neurons often migrate before undergoing final differentiation, extending neurites, and forming synaptic connections. Therefore, neuronal migration is crucial for establishing neural circuitry during development. In the developing spinal cord, neuroprogenitors first undergo radial migration within the ventricular zone. Differentiated neurons continue to migrate tangentially before reaching the final positions. The molecular pathways that regulate these migration processes remain largely unknown. Our previous study suggests that the DCC receptor is important for the migration of the dorsal spinal cord progenitors and interneurons. In this study, we determined the involvement of the Netrin1 ligand and the ROBO3 coreceptor in the migration. RESULTS: By pulse labeling neuroprogenitors with electroporation, we examined their radial migration in Netrin1 (Ntn1), Dcc, and Robo3 knockout mice. We found that all three mutants exhibit delayed migration. Furthermore, using immunohistochemistry of the BARHL2 interneuron marker, we found that the mediolateral and dorsoventral migration of differentiated dorsal interneurons is also delayed. Together, our results suggest that Netrin1/DCC signaling induce neuronal migration in the dorsal spinal cord. CONCLUSIONS: Netrin1, DCC, and ROBO3 have been extensively studied for their functions in regulating axon guidance in the spinal commissural interneurons. We reveal that during earlier development of dorsal interneurons including commissural neurons, these molecules play an important role in promoting cell migration. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13064-016-0074-x) contains supplementary material, which is available to authorized users.
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spelling pubmed-50819742016-10-28 Netrin1/DCC signaling promotes neuronal migration in the dorsal spinal cord Junge, Harald J. Yung, Andrea R. Goodrich, Lisa V. Chen, Zhe Neural Dev Short Report BACKGROUND: Newborn neurons often migrate before undergoing final differentiation, extending neurites, and forming synaptic connections. Therefore, neuronal migration is crucial for establishing neural circuitry during development. In the developing spinal cord, neuroprogenitors first undergo radial migration within the ventricular zone. Differentiated neurons continue to migrate tangentially before reaching the final positions. The molecular pathways that regulate these migration processes remain largely unknown. Our previous study suggests that the DCC receptor is important for the migration of the dorsal spinal cord progenitors and interneurons. In this study, we determined the involvement of the Netrin1 ligand and the ROBO3 coreceptor in the migration. RESULTS: By pulse labeling neuroprogenitors with electroporation, we examined their radial migration in Netrin1 (Ntn1), Dcc, and Robo3 knockout mice. We found that all three mutants exhibit delayed migration. Furthermore, using immunohistochemistry of the BARHL2 interneuron marker, we found that the mediolateral and dorsoventral migration of differentiated dorsal interneurons is also delayed. Together, our results suggest that Netrin1/DCC signaling induce neuronal migration in the dorsal spinal cord. CONCLUSIONS: Netrin1, DCC, and ROBO3 have been extensively studied for their functions in regulating axon guidance in the spinal commissural interneurons. We reveal that during earlier development of dorsal interneurons including commissural neurons, these molecules play an important role in promoting cell migration. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13064-016-0074-x) contains supplementary material, which is available to authorized users. BioMed Central 2016-10-26 /pmc/articles/PMC5081974/ /pubmed/27784329 http://dx.doi.org/10.1186/s13064-016-0074-x Text en © The Author(s). 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Short Report
Junge, Harald J.
Yung, Andrea R.
Goodrich, Lisa V.
Chen, Zhe
Netrin1/DCC signaling promotes neuronal migration in the dorsal spinal cord
title Netrin1/DCC signaling promotes neuronal migration in the dorsal spinal cord
title_full Netrin1/DCC signaling promotes neuronal migration in the dorsal spinal cord
title_fullStr Netrin1/DCC signaling promotes neuronal migration in the dorsal spinal cord
title_full_unstemmed Netrin1/DCC signaling promotes neuronal migration in the dorsal spinal cord
title_short Netrin1/DCC signaling promotes neuronal migration in the dorsal spinal cord
title_sort netrin1/dcc signaling promotes neuronal migration in the dorsal spinal cord
topic Short Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5081974/
https://www.ncbi.nlm.nih.gov/pubmed/27784329
http://dx.doi.org/10.1186/s13064-016-0074-x
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