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The molecular and cellular signatures of the mouse eminentia thalami support its role as a signalling centre in the developing forebrain

The mammalian eminentia thalami (EmT) (or thalamic eminence) is an embryonic forebrain structure of unknown function. Here, we examined the molecular and cellular properties of the mouse EmT. We first studied mRNA expression of signalling molecules and found that the EmT is a structure, rich in expr...

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Autores principales: Adutwum-Ofosu, Kevin Kofi, Magnani, Dario, Theil, Thomas, Price, David J., Fotaki, Vassiliki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5009181/
https://www.ncbi.nlm.nih.gov/pubmed/26459142
http://dx.doi.org/10.1007/s00429-015-1127-3
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author Adutwum-Ofosu, Kevin Kofi
Magnani, Dario
Theil, Thomas
Price, David J.
Fotaki, Vassiliki
author_facet Adutwum-Ofosu, Kevin Kofi
Magnani, Dario
Theil, Thomas
Price, David J.
Fotaki, Vassiliki
author_sort Adutwum-Ofosu, Kevin Kofi
collection PubMed
description The mammalian eminentia thalami (EmT) (or thalamic eminence) is an embryonic forebrain structure of unknown function. Here, we examined the molecular and cellular properties of the mouse EmT. We first studied mRNA expression of signalling molecules and found that the EmT is a structure, rich in expression of secreted factors, with Wnts being the most abundantly detected. We then examined whether EmT tissue could induce cell fate changes when grafted ectopically. For this, we transplanted EmT tissue from a tau-GFP mouse to the ventral telencephalon of a wild type host, a telencephalic region where Wnt signalling is not normally active but which we showed in culture experiments is competent to respond to Wnts. We observed that the EmT was able to induce in adjacent ventral telencephalic cells ectopic expression of Lef1, a transcriptional activator and a target gene of the Wnt/β-catenin pathway. These Lef1-positive;GFP-negative cells expressed the telencephalic marker Foxg1 but not Ascl1, which is normally expressed by ventral telencephalic cells. These results suggest that the EmT has the capacity to activate Wnt/β-catenin signalling in the ventral telencephalon and to suppress ventral telencephalic gene expression. Altogether, our data support a role of the EmT as a signalling centre in the developing mouse forebrain. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00429-015-1127-3) contains supplementary material, which is available to authorized users.
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spelling pubmed-50091812016-09-16 The molecular and cellular signatures of the mouse eminentia thalami support its role as a signalling centre in the developing forebrain Adutwum-Ofosu, Kevin Kofi Magnani, Dario Theil, Thomas Price, David J. Fotaki, Vassiliki Brain Struct Funct Original Article The mammalian eminentia thalami (EmT) (or thalamic eminence) is an embryonic forebrain structure of unknown function. Here, we examined the molecular and cellular properties of the mouse EmT. We first studied mRNA expression of signalling molecules and found that the EmT is a structure, rich in expression of secreted factors, with Wnts being the most abundantly detected. We then examined whether EmT tissue could induce cell fate changes when grafted ectopically. For this, we transplanted EmT tissue from a tau-GFP mouse to the ventral telencephalon of a wild type host, a telencephalic region where Wnt signalling is not normally active but which we showed in culture experiments is competent to respond to Wnts. We observed that the EmT was able to induce in adjacent ventral telencephalic cells ectopic expression of Lef1, a transcriptional activator and a target gene of the Wnt/β-catenin pathway. These Lef1-positive;GFP-negative cells expressed the telencephalic marker Foxg1 but not Ascl1, which is normally expressed by ventral telencephalic cells. These results suggest that the EmT has the capacity to activate Wnt/β-catenin signalling in the ventral telencephalon and to suppress ventral telencephalic gene expression. Altogether, our data support a role of the EmT as a signalling centre in the developing mouse forebrain. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00429-015-1127-3) contains supplementary material, which is available to authorized users. Springer Berlin Heidelberg 2015-10-12 2016 /pmc/articles/PMC5009181/ /pubmed/26459142 http://dx.doi.org/10.1007/s00429-015-1127-3 Text en © The Author(s) 2015 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Original Article
Adutwum-Ofosu, Kevin Kofi
Magnani, Dario
Theil, Thomas
Price, David J.
Fotaki, Vassiliki
The molecular and cellular signatures of the mouse eminentia thalami support its role as a signalling centre in the developing forebrain
title The molecular and cellular signatures of the mouse eminentia thalami support its role as a signalling centre in the developing forebrain
title_full The molecular and cellular signatures of the mouse eminentia thalami support its role as a signalling centre in the developing forebrain
title_fullStr The molecular and cellular signatures of the mouse eminentia thalami support its role as a signalling centre in the developing forebrain
title_full_unstemmed The molecular and cellular signatures of the mouse eminentia thalami support its role as a signalling centre in the developing forebrain
title_short The molecular and cellular signatures of the mouse eminentia thalami support its role as a signalling centre in the developing forebrain
title_sort molecular and cellular signatures of the mouse eminentia thalami support its role as a signalling centre in the developing forebrain
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5009181/
https://www.ncbi.nlm.nih.gov/pubmed/26459142
http://dx.doi.org/10.1007/s00429-015-1127-3
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