Restriction of neural precursor ability to respond to Nurr1 by early regional specification.

During neural development, spatially regulated expression of specific transcription factors is crucial for central nervous system (CNS) regionalization, generation of neural precursors (NPs) and subsequent differentiation of specific cell types within defined regions. A critical role in dopaminergic...

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Autores principales:	Chiara Soldati, Emanuele Cacci, Stefano Biagioni, Nicoletta Carucci, Giuseppe Lupo, Carla Perrone-Capano, Isabella Saggio, Gabriella Augusti-Tocco
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/3bbb355d087f42ee9193bac92b38e408
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spelling	oai:doaj.org-article:3bbb355d087f42ee9193bac92b38e4082021-11-18T08:05:31ZRestriction of neural precursor ability to respond to Nurr1 by early regional specification.1932-620310.1371/journal.pone.0051798https://doaj.org/article/3bbb355d087f42ee9193bac92b38e4082012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23240065/?tool=EBIhttps://doaj.org/toc/1932-6203During neural development, spatially regulated expression of specific transcription factors is crucial for central nervous system (CNS) regionalization, generation of neural precursors (NPs) and subsequent differentiation of specific cell types within defined regions. A critical role in dopaminergic differentiation in the midbrain (MB) has been assigned to the transcription factor Nurr1. Nurr1 controls the expression of key genes involved in dopamine (DA) neurotransmission, e.g. tyrosine hydroxylase (TH) and the DA transporter (DAT), and promotes the dopaminergic phenotype in embryonic stem cells. We investigated whether cells derived from different areas of the mouse CNS could be directed to differentiate into dopaminergic neurons in vitro by forced expression of the transcription factor Nurr1. We show that Nurr1 overexpression can promote dopaminergic cell fate specification only in NPs obtained from E13.5 ganglionic eminence (GE) and MB, but not in NPs isolated from E13.5 cortex (CTX) and spinal cord (SC) or from the adult subventricular zone (SVZ). Confirming previous studies, we also show that Nurr1 overexpression can increase the generation of TH-positive neurons in mouse embryonic stem cells. These data show that Nurr1 ability to induce a dopaminergic phenotype becomes restricted during CNS development and is critically dependent on the region of NPs derivation. Our results suggest that the plasticity of NPs and their ability to activate a dopaminergic differentiation program in response to Nurr1 is regulated during early stages of neurogenesis, possibly through mechanisms controlling CNS regionalization.Chiara SoldatiEmanuele CacciStefano BiagioniNicoletta CarucciGiuseppe LupoCarla Perrone-CapanoIsabella SaggioGabriella Augusti-ToccoPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 12, p e51798 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Chiara Soldati Emanuele Cacci Stefano Biagioni Nicoletta Carucci Giuseppe Lupo Carla Perrone-Capano Isabella Saggio Gabriella Augusti-Tocco Restriction of neural precursor ability to respond to Nurr1 by early regional specification.
description	During neural development, spatially regulated expression of specific transcription factors is crucial for central nervous system (CNS) regionalization, generation of neural precursors (NPs) and subsequent differentiation of specific cell types within defined regions. A critical role in dopaminergic differentiation in the midbrain (MB) has been assigned to the transcription factor Nurr1. Nurr1 controls the expression of key genes involved in dopamine (DA) neurotransmission, e.g. tyrosine hydroxylase (TH) and the DA transporter (DAT), and promotes the dopaminergic phenotype in embryonic stem cells. We investigated whether cells derived from different areas of the mouse CNS could be directed to differentiate into dopaminergic neurons in vitro by forced expression of the transcription factor Nurr1. We show that Nurr1 overexpression can promote dopaminergic cell fate specification only in NPs obtained from E13.5 ganglionic eminence (GE) and MB, but not in NPs isolated from E13.5 cortex (CTX) and spinal cord (SC) or from the adult subventricular zone (SVZ). Confirming previous studies, we also show that Nurr1 overexpression can increase the generation of TH-positive neurons in mouse embryonic stem cells. These data show that Nurr1 ability to induce a dopaminergic phenotype becomes restricted during CNS development and is critically dependent on the region of NPs derivation. Our results suggest that the plasticity of NPs and their ability to activate a dopaminergic differentiation program in response to Nurr1 is regulated during early stages of neurogenesis, possibly through mechanisms controlling CNS regionalization.
format	article
author	Chiara Soldati Emanuele Cacci Stefano Biagioni Nicoletta Carucci Giuseppe Lupo Carla Perrone-Capano Isabella Saggio Gabriella Augusti-Tocco
author_facet	Chiara Soldati Emanuele Cacci Stefano Biagioni Nicoletta Carucci Giuseppe Lupo Carla Perrone-Capano Isabella Saggio Gabriella Augusti-Tocco
author_sort	Chiara Soldati
title	Restriction of neural precursor ability to respond to Nurr1 by early regional specification.
title_short	Restriction of neural precursor ability to respond to Nurr1 by early regional specification.
title_full	Restriction of neural precursor ability to respond to Nurr1 by early regional specification.
title_fullStr	Restriction of neural precursor ability to respond to Nurr1 by early regional specification.
title_full_unstemmed	Restriction of neural precursor ability to respond to Nurr1 by early regional specification.
title_sort	restriction of neural precursor ability to respond to nurr1 by early regional specification.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/3bbb355d087f42ee9193bac92b38e408
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Restriction of neural precursor ability to respond to Nurr1 by early regional specification.

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