Non cell-autonomous role of DCC in the guidance of the corticospinal tract at the midline

Abstract DCC, a NETRIN-1 receptor, is considered as a cell-autonomous regulator for midline guidance of many commissural populations in the central nervous system. The corticospinal tract (CST), the principal motor pathway for voluntary movements, crosses the anatomic midline at the pyramidal decuss...

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Autores principales:	Quentin Welniarz, Marie-Pierre Morel, Oriane Pourchet, Cécile Gallea, Jean-Charles Lamy, Massimo Cincotta, Mohamed Doulazmi, Morgane Belle, Aurélie Méneret, Oriane Trouillard, Marta Ruiz, Vanessa Brochard, Sabine Meunier, Alain Trembleau, Marie Vidailhet, Alain Chédotal, Isabelle Dusart, Emmanuel Roze
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/f624def1706f400fa3c4dcfb5662d7a0
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spelling	oai:doaj.org-article:f624def1706f400fa3c4dcfb5662d7a02021-12-02T12:32:05ZNon cell-autonomous role of DCC in the guidance of the corticospinal tract at the midline10.1038/s41598-017-00514-z2045-2322https://doaj.org/article/f624def1706f400fa3c4dcfb5662d7a02017-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-00514-zhttps://doaj.org/toc/2045-2322Abstract DCC, a NETRIN-1 receptor, is considered as a cell-autonomous regulator for midline guidance of many commissural populations in the central nervous system. The corticospinal tract (CST), the principal motor pathway for voluntary movements, crosses the anatomic midline at the pyramidal decussation. CST fails to cross the midline in Kanga mice expressing a truncated DCC protein. Humans with heterozygous DCC mutations have congenital mirror movements (CMM). As CMM has been associated, in some cases, with malformations of the pyramidal decussation, DCC might also be involved in this process in human. Here, we investigated the role of DCC in CST midline crossing both in human and mice. First, we demonstrate by multimodal approaches, that patients with CMM due to DCC mutations have an increased proportion of ipsilateral CST projections. Second, we show that in contrast to Kanga mice, the anatomy of the CST is not altered in mice with a deletion of DCC in the CST. Altogether, these results indicate that DCC controls CST midline crossing in both humans and mice, and that this process is non cell-autonomous in mice. Our data unravel a new level of complexity in the role of DCC in CST guidance at the midline.Quentin WelniarzMarie-Pierre MorelOriane PourchetCécile GalleaJean-Charles LamyMassimo CincottaMohamed DoulazmiMorgane BelleAurélie MéneretOriane TrouillardMarta RuizVanessa BrochardSabine MeunierAlain TrembleauMarie VidailhetAlain ChédotalIsabelle DusartEmmanuel RozeNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-14 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Quentin Welniarz Marie-Pierre Morel Oriane Pourchet Cécile Gallea Jean-Charles Lamy Massimo Cincotta Mohamed Doulazmi Morgane Belle Aurélie Méneret Oriane Trouillard Marta Ruiz Vanessa Brochard Sabine Meunier Alain Trembleau Marie Vidailhet Alain Chédotal Isabelle Dusart Emmanuel Roze Non cell-autonomous role of DCC in the guidance of the corticospinal tract at the midline
description	Abstract DCC, a NETRIN-1 receptor, is considered as a cell-autonomous regulator for midline guidance of many commissural populations in the central nervous system. The corticospinal tract (CST), the principal motor pathway for voluntary movements, crosses the anatomic midline at the pyramidal decussation. CST fails to cross the midline in Kanga mice expressing a truncated DCC protein. Humans with heterozygous DCC mutations have congenital mirror movements (CMM). As CMM has been associated, in some cases, with malformations of the pyramidal decussation, DCC might also be involved in this process in human. Here, we investigated the role of DCC in CST midline crossing both in human and mice. First, we demonstrate by multimodal approaches, that patients with CMM due to DCC mutations have an increased proportion of ipsilateral CST projections. Second, we show that in contrast to Kanga mice, the anatomy of the CST is not altered in mice with a deletion of DCC in the CST. Altogether, these results indicate that DCC controls CST midline crossing in both humans and mice, and that this process is non cell-autonomous in mice. Our data unravel a new level of complexity in the role of DCC in CST guidance at the midline.
format	article
author	Quentin Welniarz Marie-Pierre Morel Oriane Pourchet Cécile Gallea Jean-Charles Lamy Massimo Cincotta Mohamed Doulazmi Morgane Belle Aurélie Méneret Oriane Trouillard Marta Ruiz Vanessa Brochard Sabine Meunier Alain Trembleau Marie Vidailhet Alain Chédotal Isabelle Dusart Emmanuel Roze
author_facet	Quentin Welniarz Marie-Pierre Morel Oriane Pourchet Cécile Gallea Jean-Charles Lamy Massimo Cincotta Mohamed Doulazmi Morgane Belle Aurélie Méneret Oriane Trouillard Marta Ruiz Vanessa Brochard Sabine Meunier Alain Trembleau Marie Vidailhet Alain Chédotal Isabelle Dusart Emmanuel Roze
author_sort	Quentin Welniarz
title	Non cell-autonomous role of DCC in the guidance of the corticospinal tract at the midline
title_short	Non cell-autonomous role of DCC in the guidance of the corticospinal tract at the midline
title_full	Non cell-autonomous role of DCC in the guidance of the corticospinal tract at the midline
title_fullStr	Non cell-autonomous role of DCC in the guidance of the corticospinal tract at the midline
title_full_unstemmed	Non cell-autonomous role of DCC in the guidance of the corticospinal tract at the midline
title_sort	non cell-autonomous role of dcc in the guidance of the corticospinal tract at the midline
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/f624def1706f400fa3c4dcfb5662d7a0
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Non cell-autonomous role of DCC in the guidance of the corticospinal tract at the midline

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