Molecular mechanism of central nervous system repair by the Drosophila NG2 homologue kon-tiki

Neuron glia antigen 2 (NG2)–positive glia are repair cells that proliferate upon central nervous system (CNS) damage, promoting functional recovery. However, repair is limited because of the failure of the newly produced glial cells to differentiate. It is a key goal to discover how to regulate NG2...

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Detalhes bibliográficos
Autores: Losada Pérez, María De La Paloma, Harrison, Neale, Hidalgo, Alicia
Formato: artículo
Fecha de publicación:2016
País:España
Recursos:Universidad Complutense de Madrid (UCM)
Repositorio:Docta Complutense
Idioma:inglés
OAI Identifier:oai:docta.ucm.es:20.500.14352/94805
Acesso em linha:https://hdl.handle.net/20.500.14352/94805
Access Level:acceso abierto
Palavra-chave:612.82
Neurociencias (Biológicas)
2415 Biología Molecular
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spelling Molecular mechanism of central nervous system repair by the Drosophila NG2 homologue kon-tikiLosada Pérez, María De La PalomaHarrison, NealeHidalgo, Alicia612.82Neurociencias (Biológicas)2415 Biología MolecularNeuron glia antigen 2 (NG2)–positive glia are repair cells that proliferate upon central nervous system (CNS) damage, promoting functional recovery. However, repair is limited because of the failure of the newly produced glial cells to differentiate. It is a key goal to discover how to regulate NG2 to enable glial proliferation and differentiation conducive to repair. Drosophila has an NG2 homologue called kon-tiki (kon), of unknown CNS function. We show that kon promotes repair and identify the underlying mechanism. Crush injury up-regulates kon expression downstream of Notch. Kon in turn induces glial proliferation and initiates glial differentiation by activating glial genes and prospero (pros). Two negative feedback loops with Notch and Pros allow Kon to drive the homeostatic regulation required for repair. By modulating Kon levels in glia, we could prevent or promote CNS repair. Thus, the functional links between Kon, Notch, and Pros are essential for, and can drive, repair. Analogous mechanisms could promote CNS repair in mammals.Rockefeller University PressUniversidad Complutense de Madrid20162016-01-0120162016-01-01journal articlehttp://purl.org/coar/resource_type/c_6501VoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttps://hdl.handle.net/20.500.14352/94805reponame:Docta Complutenseinstname:Universidad Complutense de Madrid (UCM)Inglésengopen accesshttp://purl.org/coar/access_right/c_abf2Attribution-NoDerivatives 4.0 Internationalhttp://creativecommons.org/licenses/by-nd/4.0/info:eu-repo/semantics/openAccessoai:docta.ucm.es:20.500.14352/948052026-06-02T12:44:21Z
dc.title.none.fl_str_mv Molecular mechanism of central nervous system repair by the Drosophila NG2 homologue kon-tiki
title Molecular mechanism of central nervous system repair by the Drosophila NG2 homologue kon-tiki
spellingShingle Molecular mechanism of central nervous system repair by the Drosophila NG2 homologue kon-tiki
Losada Pérez, María De La Paloma
612.82
Neurociencias (Biológicas)
2415 Biología Molecular
title_short Molecular mechanism of central nervous system repair by the Drosophila NG2 homologue kon-tiki
title_full Molecular mechanism of central nervous system repair by the Drosophila NG2 homologue kon-tiki
title_fullStr Molecular mechanism of central nervous system repair by the Drosophila NG2 homologue kon-tiki
title_full_unstemmed Molecular mechanism of central nervous system repair by the Drosophila NG2 homologue kon-tiki
title_sort Molecular mechanism of central nervous system repair by the Drosophila NG2 homologue kon-tiki
dc.creator.none.fl_str_mv Losada Pérez, María De La Paloma
Harrison, Neale
Hidalgo, Alicia
author Losada Pérez, María De La Paloma
author_facet Losada Pérez, María De La Paloma
Harrison, Neale
Hidalgo, Alicia
author_role author
author2 Harrison, Neale
Hidalgo, Alicia
author2_role author
author
dc.contributor.none.fl_str_mv Universidad Complutense de Madrid
dc.subject.none.fl_str_mv 612.82
Neurociencias (Biológicas)
2415 Biología Molecular
topic 612.82
Neurociencias (Biológicas)
2415 Biología Molecular
description Neuron glia antigen 2 (NG2)–positive glia are repair cells that proliferate upon central nervous system (CNS) damage, promoting functional recovery. However, repair is limited because of the failure of the newly produced glial cells to differentiate. It is a key goal to discover how to regulate NG2 to enable glial proliferation and differentiation conducive to repair. Drosophila has an NG2 homologue called kon-tiki (kon), of unknown CNS function. We show that kon promotes repair and identify the underlying mechanism. Crush injury up-regulates kon expression downstream of Notch. Kon in turn induces glial proliferation and initiates glial differentiation by activating glial genes and prospero (pros). Two negative feedback loops with Notch and Pros allow Kon to drive the homeostatic regulation required for repair. By modulating Kon levels in glia, we could prevent or promote CNS repair. Thus, the functional links between Kon, Notch, and Pros are essential for, and can drive, repair. Analogous mechanisms could promote CNS repair in mammals.
publishDate 2016
dc.date.none.fl_str_mv 2016
2016-01-01
2016
2016-01-01
dc.type.none.fl_str_mv journal article
http://purl.org/coar/resource_type/c_6501
VoR
http://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv https://hdl.handle.net/20.500.14352/94805
url https://hdl.handle.net/20.500.14352/94805
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
Attribution-NoDerivatives 4.0 International
http://creativecommons.org/licenses/by-nd/4.0/
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
Attribution-NoDerivatives 4.0 International
http://creativecommons.org/licenses/by-nd/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Rockefeller University Press
publisher.none.fl_str_mv Rockefeller University Press
dc.source.none.fl_str_mv reponame:Docta Complutense
instname:Universidad Complutense de Madrid (UCM)
instname_str Universidad Complutense de Madrid (UCM)
reponame_str Docta Complutense
collection Docta Complutense
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,301603

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