Sim1 is required for the migration and axonal projections of V3 interneurons in the developing mouse spinal cord

Autores
Blacklaws, Jake; Deska Gauthier, Dylan; Jones, Christopher T.; Petracca, Yanina Luján; Liu, Mingwei; Zhang, Han; Fawcett, James P.; Glover, Joel C.; Lanuza, Guillermo Marcos; Zhang, Ying
Año de publicación
2015
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
V3 spinal interneurons (INs) are a group of excitatory INs that play a crucial role in producing balanced and stable gaits in vertebrate animals. In the developing mouse spinal cord, V3 INs arise from the most ventral progenitor domain and form anatomically distinctive subpopulations in adult spinal cords. They are marked by the expression of transcription factor Sim1 postmitotically, but the function of Sim1 in V3 development remains unknown. Here, we used Sim1(Cre) ;tdTomato mice to trace the fate of V3 INs in a Sim1 mutant versus control genetic background during development. In Sim1 mutants, V3 INs are produced normally and maintain a similar position and organization as in wild types before E12.5. Further temporal analysis revealed that the V3 INs in the mutants failed to migrate properly to form V3 subgroups along the dorsoventral axis of the spinal cord. At birth, in the Sim1 mutant the number of V3 INs in the ventral subgroup was normal, but they were significantly reduced in the dorsal subgroup with a concomitant increase in the intermediate subgroup. Retrograde labeling at lumbar level revealed that loss of Sim1 led to a reduction in extension of contralateral axon projections both at E14.5 and P0 without affecting ipsilateral axon projections. These results demonstrate that Sim1 is essential for proper migration and the guidance of commissural axons of the spinal V3 INs.
Fil: Blacklaws, Jake. Dalhousie University Halifax; Canadá
Fil: Deska Gauthier, Dylan. Dalhousie University Halifax; Canadá
Fil: Jones, Christopher T.. Dalhousie University Halifax; Canadá
Fil: Petracca, Yanina Luján. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina
Fil: Liu, Mingwei. Dalhousie University Halifax; Canadá
Fil: Zhang, Han. Dalhousie University Halifax; Canadá
Fil: Fawcett, James P.. Dalhousie University Halifax; Canadá
Fil: Glover, Joel C.. University of Oslo; Noruega
Fil: Lanuza, Guillermo Marcos. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina
Fil: Zhang, Ying. Dalhousie University Halifax; Canadá
Materia
Spinal Cord
Axonal Projection
Migration
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/24467
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/24467
network_acronym_str CONICETDig
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network_name_str CONICET Digital (CONICET)
spelling Sim1 is required for the migration and axonal projections of V3 interneurons in the developing mouse spinal cordBlacklaws, JakeDeska Gauthier, DylanJones, Christopher T.Petracca, Yanina LujánLiu, MingweiZhang, HanFawcett, James P.Glover, Joel C.Lanuza, Guillermo MarcosZhang, YingSpinal CordAxonal ProjectionMigrationhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3V3 spinal interneurons (INs) are a group of excitatory INs that play a crucial role in producing balanced and stable gaits in vertebrate animals. In the developing mouse spinal cord, V3 INs arise from the most ventral progenitor domain and form anatomically distinctive subpopulations in adult spinal cords. They are marked by the expression of transcription factor Sim1 postmitotically, but the function of Sim1 in V3 development remains unknown. Here, we used Sim1(Cre) ;tdTomato mice to trace the fate of V3 INs in a Sim1 mutant versus control genetic background during development. In Sim1 mutants, V3 INs are produced normally and maintain a similar position and organization as in wild types before E12.5. Further temporal analysis revealed that the V3 INs in the mutants failed to migrate properly to form V3 subgroups along the dorsoventral axis of the spinal cord. At birth, in the Sim1 mutant the number of V3 INs in the ventral subgroup was normal, but they were significantly reduced in the dorsal subgroup with a concomitant increase in the intermediate subgroup. Retrograde labeling at lumbar level revealed that loss of Sim1 led to a reduction in extension of contralateral axon projections both at E14.5 and P0 without affecting ipsilateral axon projections. These results demonstrate that Sim1 is essential for proper migration and the guidance of commissural axons of the spinal V3 INs.Fil: Blacklaws, Jake. Dalhousie University Halifax; CanadáFil: Deska Gauthier, Dylan. Dalhousie University Halifax; CanadáFil: Jones, Christopher T.. Dalhousie University Halifax; CanadáFil: Petracca, Yanina Luján. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; ArgentinaFil: Liu, Mingwei. Dalhousie University Halifax; CanadáFil: Zhang, Han. Dalhousie University Halifax; CanadáFil: Fawcett, James P.. Dalhousie University Halifax; CanadáFil: Glover, Joel C.. University of Oslo; NoruegaFil: Lanuza, Guillermo Marcos. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; ArgentinaFil: Zhang, Ying. Dalhousie University Halifax; CanadáWiley2015-02info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/24467Blacklaws, Jake; Deska Gauthier, Dylan; Jones, Christopher T.; Petracca, Yanina Luján; Liu, Mingwei; et al.; Sim1 is required for the migration and axonal projections of V3 interneurons in the developing mouse spinal cord; Wiley; Developmental Neurobiology; 75; 9; 2-2015; 1003-10171932-84511932-846XCONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://onlinelibrary.wiley.com/doi/10.1002/dneu.22266/abstractinfo:eu-repo/semantics/altIdentifier/doi/10.1002/dneu.22266info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:01:31Zoai:ri.conicet.gov.ar:11336/24467instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 10:01:31.462CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Sim1 is required for the migration and axonal projections of V3 interneurons in the developing mouse spinal cord
title Sim1 is required for the migration and axonal projections of V3 interneurons in the developing mouse spinal cord
spellingShingle Sim1 is required for the migration and axonal projections of V3 interneurons in the developing mouse spinal cord
Blacklaws, Jake
Spinal Cord
Axonal Projection
Migration
title_short Sim1 is required for the migration and axonal projections of V3 interneurons in the developing mouse spinal cord
title_full Sim1 is required for the migration and axonal projections of V3 interneurons in the developing mouse spinal cord
title_fullStr Sim1 is required for the migration and axonal projections of V3 interneurons in the developing mouse spinal cord
title_full_unstemmed Sim1 is required for the migration and axonal projections of V3 interneurons in the developing mouse spinal cord
title_sort Sim1 is required for the migration and axonal projections of V3 interneurons in the developing mouse spinal cord
dc.creator.none.fl_str_mv Blacklaws, Jake
Deska Gauthier, Dylan
Jones, Christopher T.
Petracca, Yanina Luján
Liu, Mingwei
Zhang, Han
Fawcett, James P.
Glover, Joel C.
Lanuza, Guillermo Marcos
Zhang, Ying
author Blacklaws, Jake
author_facet Blacklaws, Jake
Deska Gauthier, Dylan
Jones, Christopher T.
Petracca, Yanina Luján
Liu, Mingwei
Zhang, Han
Fawcett, James P.
Glover, Joel C.
Lanuza, Guillermo Marcos
Zhang, Ying
author_role author
author2 Deska Gauthier, Dylan
Jones, Christopher T.
Petracca, Yanina Luján
Liu, Mingwei
Zhang, Han
Fawcett, James P.
Glover, Joel C.
Lanuza, Guillermo Marcos
Zhang, Ying
author2_role author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Spinal Cord
Axonal Projection
Migration
topic Spinal Cord
Axonal Projection
Migration
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv V3 spinal interneurons (INs) are a group of excitatory INs that play a crucial role in producing balanced and stable gaits in vertebrate animals. In the developing mouse spinal cord, V3 INs arise from the most ventral progenitor domain and form anatomically distinctive subpopulations in adult spinal cords. They are marked by the expression of transcription factor Sim1 postmitotically, but the function of Sim1 in V3 development remains unknown. Here, we used Sim1(Cre) ;tdTomato mice to trace the fate of V3 INs in a Sim1 mutant versus control genetic background during development. In Sim1 mutants, V3 INs are produced normally and maintain a similar position and organization as in wild types before E12.5. Further temporal analysis revealed that the V3 INs in the mutants failed to migrate properly to form V3 subgroups along the dorsoventral axis of the spinal cord. At birth, in the Sim1 mutant the number of V3 INs in the ventral subgroup was normal, but they were significantly reduced in the dorsal subgroup with a concomitant increase in the intermediate subgroup. Retrograde labeling at lumbar level revealed that loss of Sim1 led to a reduction in extension of contralateral axon projections both at E14.5 and P0 without affecting ipsilateral axon projections. These results demonstrate that Sim1 is essential for proper migration and the guidance of commissural axons of the spinal V3 INs.
Fil: Blacklaws, Jake. Dalhousie University Halifax; Canadá
Fil: Deska Gauthier, Dylan. Dalhousie University Halifax; Canadá
Fil: Jones, Christopher T.. Dalhousie University Halifax; Canadá
Fil: Petracca, Yanina Luján. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina
Fil: Liu, Mingwei. Dalhousie University Halifax; Canadá
Fil: Zhang, Han. Dalhousie University Halifax; Canadá
Fil: Fawcett, James P.. Dalhousie University Halifax; Canadá
Fil: Glover, Joel C.. University of Oslo; Noruega
Fil: Lanuza, Guillermo Marcos. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina
Fil: Zhang, Ying. Dalhousie University Halifax; Canadá
description V3 spinal interneurons (INs) are a group of excitatory INs that play a crucial role in producing balanced and stable gaits in vertebrate animals. In the developing mouse spinal cord, V3 INs arise from the most ventral progenitor domain and form anatomically distinctive subpopulations in adult spinal cords. They are marked by the expression of transcription factor Sim1 postmitotically, but the function of Sim1 in V3 development remains unknown. Here, we used Sim1(Cre) ;tdTomato mice to trace the fate of V3 INs in a Sim1 mutant versus control genetic background during development. In Sim1 mutants, V3 INs are produced normally and maintain a similar position and organization as in wild types before E12.5. Further temporal analysis revealed that the V3 INs in the mutants failed to migrate properly to form V3 subgroups along the dorsoventral axis of the spinal cord. At birth, in the Sim1 mutant the number of V3 INs in the ventral subgroup was normal, but they were significantly reduced in the dorsal subgroup with a concomitant increase in the intermediate subgroup. Retrograde labeling at lumbar level revealed that loss of Sim1 led to a reduction in extension of contralateral axon projections both at E14.5 and P0 without affecting ipsilateral axon projections. These results demonstrate that Sim1 is essential for proper migration and the guidance of commissural axons of the spinal V3 INs.
publishDate 2015
dc.date.none.fl_str_mv 2015-02
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/24467
Blacklaws, Jake; Deska Gauthier, Dylan; Jones, Christopher T.; Petracca, Yanina Luján; Liu, Mingwei; et al.; Sim1 is required for the migration and axonal projections of V3 interneurons in the developing mouse spinal cord; Wiley; Developmental Neurobiology; 75; 9; 2-2015; 1003-1017
1932-8451
1932-846X
CONICET Digital
CONICET
url http://hdl.handle.net/11336/24467
identifier_str_mv Blacklaws, Jake; Deska Gauthier, Dylan; Jones, Christopher T.; Petracca, Yanina Luján; Liu, Mingwei; et al.; Sim1 is required for the migration and axonal projections of V3 interneurons in the developing mouse spinal cord; Wiley; Developmental Neurobiology; 75; 9; 2-2015; 1003-1017
1932-8451
1932-846X
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://onlinelibrary.wiley.com/doi/10.1002/dneu.22266/abstract
info:eu-repo/semantics/altIdentifier/doi/10.1002/dneu.22266
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Wiley
publisher.none.fl_str_mv Wiley
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.13397

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