NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of Notch
Notch and neurotrophins control neuronal shape, but it is not known whether their signaling pathways intersect. Here we report results from hippocampal neuronal cultures that are in support of this possibility. We found that low cell density or blockade of Notch signaling by a soluble Delta-Fc ligan...
| Autores: | , , , , |
|---|---|
| Formato: | artículo |
| Fecha de publicación: | 2005 |
| País: | España |
| Recursos: | Consejo Superior de Investigaciones Científicas (CSIC) |
| Repositorio: | DIGITAL.CSIC. Repositorio Institucional del CSIC |
| OAI Identifier: | oai:digital.csic.es:10261/150408 |
| Acesso em linha: | http://hdl.handle.net/10261/150408 |
| Access Level: | acceso abierto |
| id |
ES_490cdeb58fa095f78df6cc56c05b08ac |
|---|---|
| oai_identifier_str |
oai:digital.csic.es:10261/150408 |
| network_acronym_str |
ES |
| network_name_str |
España |
| repository_id_str |
|
| spelling |
NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of NotchSalama-Cohen, P.Arévalo, María ÁngelesMeier, J.Grantyn, R.Rodríguez-Tebar, AlfredoNotch and neurotrophins control neuronal shape, but it is not known whether their signaling pathways intersect. Here we report results from hippocampal neuronal cultures that are in support of this possibility. We found that low cell density or blockade of Notch signaling by a soluble Delta-Fc ligand decreased the mRNA levels of the nuclear targets of Notch, the homologues of enhancer-of-split 1 and 5 (Hes1/5). This effect was associated with enhanced sprouting of new dendrites or dendrite branches. In contrast, high cell density or exposure of low-density cultures to NGF increased the Hes1/5 mRNA, reduced the number of primary dendrites and promoted dendrite elongation. The NGF effects on both Hes1/5 expression and dendrite morphology were prevented by p75-antibody (a p75NTR-blocking antibody) or transfection with enhancer-of-split 6 (Hes6), a condition known to suppress Hes activity. Nuclear translocation of NF-kappaB was identified as a link between p75NTR and Hes1/5 because it was required for the up-regulation of these two genes. The convergence of the Notch and p75NTR signaling pathways at the level of Hes1/5 illuminates an unexpected mechanism through which a diffusible factor (NGF) could regulate dendrite growth when cell-cell interaction via Notch is not in action.Peer ReviewedAmerican Society for Cell BiologyConsejo Superior de Investigaciones Científicas [https://ror.org/02gfc7t72]2017201720052017info:eu-repo/semantics/articlehttp://purl.org/coar/resource_type/c_6501http://hdl.handle.net/10261/150408reponame:DIGITAL.CSIC. Repositorio Institucional del CSICinstname:Consejo Superior de Investigaciones Científicas (CSIC)InglésSíinfo:eu-repo/semantics/openAccessoai:digital.csic.es:10261/1504082026-05-22T06:33:51Z |
| dc.title.none.fl_str_mv |
NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of Notch |
| title |
NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of Notch |
| spellingShingle |
NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of Notch Salama-Cohen, P. |
| title_short |
NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of Notch |
| title_full |
NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of Notch |
| title_fullStr |
NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of Notch |
| title_full_unstemmed |
NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of Notch |
| title_sort |
NGF controls dendrite development in hippocampal neurons by binding to p75NTR and modulating the cellular targets of Notch |
| dc.creator.none.fl_str_mv |
Salama-Cohen, P. Arévalo, María Ángeles Meier, J. Grantyn, R. Rodríguez-Tebar, Alfredo |
| author |
Salama-Cohen, P. |
| author_facet |
Salama-Cohen, P. Arévalo, María Ángeles Meier, J. Grantyn, R. Rodríguez-Tebar, Alfredo |
| author_role |
author |
| author2 |
Arévalo, María Ángeles Meier, J. Grantyn, R. Rodríguez-Tebar, Alfredo |
| author2_role |
author author author author |
| dc.contributor.none.fl_str_mv |
Consejo Superior de Investigaciones Científicas [https://ror.org/02gfc7t72] |
| description |
Notch and neurotrophins control neuronal shape, but it is not known whether their signaling pathways intersect. Here we report results from hippocampal neuronal cultures that are in support of this possibility. We found that low cell density or blockade of Notch signaling by a soluble Delta-Fc ligand decreased the mRNA levels of the nuclear targets of Notch, the homologues of enhancer-of-split 1 and 5 (Hes1/5). This effect was associated with enhanced sprouting of new dendrites or dendrite branches. In contrast, high cell density or exposure of low-density cultures to NGF increased the Hes1/5 mRNA, reduced the number of primary dendrites and promoted dendrite elongation. The NGF effects on both Hes1/5 expression and dendrite morphology were prevented by p75-antibody (a p75NTR-blocking antibody) or transfection with enhancer-of-split 6 (Hes6), a condition known to suppress Hes activity. Nuclear translocation of NF-kappaB was identified as a link between p75NTR and Hes1/5 because it was required for the up-regulation of these two genes. The convergence of the Notch and p75NTR signaling pathways at the level of Hes1/5 illuminates an unexpected mechanism through which a diffusible factor (NGF) could regulate dendrite growth when cell-cell interaction via Notch is not in action. |
| publishDate |
2005 |
| dc.date.none.fl_str_mv |
2005 2017 2017 2017 |
| dc.type.none.fl_str_mv |
info:eu-repo/semantics/article http://purl.org/coar/resource_type/c_6501 |
| format |
article |
| dc.identifier.none.fl_str_mv |
http://hdl.handle.net/10261/150408 |
| url |
http://hdl.handle.net/10261/150408 |
| dc.language.none.fl_str_mv |
Inglés |
| language_invalid_str_mv |
Inglés |
| dc.relation.none.fl_str_mv |
Sí |
| dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess |
| eu_rights_str_mv |
openAccess |
| dc.publisher.none.fl_str_mv |
American Society for Cell Biology |
| publisher.none.fl_str_mv |
American Society for Cell Biology |
| dc.source.none.fl_str_mv |
reponame:DIGITAL.CSIC. Repositorio Institucional del CSIC instname:Consejo Superior de Investigaciones Científicas (CSIC) |
| instname_str |
Consejo Superior de Investigaciones Científicas (CSIC) |
| reponame_str |
DIGITAL.CSIC. Repositorio Institucional del CSIC |
| collection |
DIGITAL.CSIC. Repositorio Institucional del CSIC |
| repository.name.fl_str_mv |
|
| repository.mail.fl_str_mv |
|
| _version_ |
1869407398110691328 |
| score |
15,812429 |