Proliferative Defects and Formation of a Double Cortex in Mice Lacking Mltt4 and Cdh2 in the Dorsal Telencephalon

Radial glial cells (RGCs) in the ventricular neuroepithelium of the dorsal telencephalon are the progenitor cells for neocortical projection neurons and astrocytes. Here we showthatthe adherens junction proteins afadin and CDH2 are criticalforthe control of cell proliferation in the dorsal telencep...

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Principais autores:	Gil-Sanz, Cristina, Landeira, Bruna, Ramos, Cynthia, Costa, Marcos Romualdo, Müller, Ulrich
Formato:	article
Idioma:	eng
Publicado em:	The Journal of Neuroscience
Assuntos:	afadin CDH2 double cortex neocortex progenitor radial glia
Endereço do item:	https://repositorio.ufrn.br/jspui/handle/1/11823
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id	ri-1-11823
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spelling	ri-1-118232021-07-09T20:30:22Z Proliferative Defects and Formation of a Double Cortex in Mice Lacking Mltt4 and Cdh2 in the Dorsal Telencephalon Gil-Sanz, Cristina Landeira, Bruna Ramos, Cynthia Costa, Marcos Romualdo Müller, Ulrich afadin CDH2 double cortex neocortex progenitor radial glia Radial glial cells (RGCs) in the ventricular neuroepithelium of the dorsal telencephalon are the progenitor cells for neocortical projection neurons and astrocytes. Here we showthatthe adherens junction proteins afadin and CDH2 are criticalforthe control of cell proliferation in the dorsal telencephalon and for the formation of its normal laminar structure. Inactivation of afadin or CDH2 in the dorsal telenceph-alon leads to a phenotype resembling subcortical band heterotopia, also known as “double cortex,” a brain malformation in which heterotopic gray matter is interposed between zones of white matter. Adherens junctions between RGCs are disrupted in the mutants, progenitor cells are widely dispersed throughout the developing neocortex, and their proliferation is dramatically increased. Major subtypes of neocortical projection neurons are generated, but their integration into cell layers is disrupted. Our findings suggest that defects in adherens junctions components in mice massively affects progenitor cell proliferation and leads to a double cortex-like phenotype. 2014-08-13T14:00:46Z 2014-08-13T14:00:46Z 2014-08-06 article Gil-Sanz, Cristina; Landeira, Bruna; Ramos, Cynthia; Costa, Marcos R.; Müller, Ulrich. Proliferative Defects and Formation of a Double Cortex in Mice Lacking Mltt4 and Cdh2 in the Dorsal Telencephalon. The Journal of Neuroscience, v.34, n.2, 6 Ago. 2014, p.10475–10487. https://repositorio.ufrn.br/jspui/handle/1/11823 eng Acesso Aberto application/pdf The Journal of Neuroscience
institution	Repositório Institucional
collection	RI - UFRN
language	eng
topic	afadin CDH2 double cortex neocortex progenitor radial glia
spellingShingle	afadin CDH2 double cortex neocortex progenitor radial glia Gil-Sanz, Cristina Landeira, Bruna Ramos, Cynthia Costa, Marcos Romualdo Müller, Ulrich Proliferative Defects and Formation of a Double Cortex in Mice Lacking Mltt4 and Cdh2 in the Dorsal Telencephalon
description	Radial glial cells (RGCs) in the ventricular neuroepithelium of the dorsal telencephalon are the progenitor cells for neocortical projection neurons and astrocytes. Here we showthatthe adherens junction proteins afadin and CDH2 are criticalforthe control of cell proliferation in the dorsal telencephalon and for the formation of its normal laminar structure. Inactivation of afadin or CDH2 in the dorsal telenceph-alon leads to a phenotype resembling subcortical band heterotopia, also known as “double cortex,” a brain malformation in which heterotopic gray matter is interposed between zones of white matter. Adherens junctions between RGCs are disrupted in the mutants, progenitor cells are widely dispersed throughout the developing neocortex, and their proliferation is dramatically increased. Major subtypes of neocortical projection neurons are generated, but their integration into cell layers is disrupted. Our findings suggest that defects in adherens junctions components in mice massively affects progenitor cell proliferation and leads to a double cortex-like phenotype.
format	article
author	Gil-Sanz, Cristina Landeira, Bruna Ramos, Cynthia Costa, Marcos Romualdo Müller, Ulrich
author_facet	Gil-Sanz, Cristina Landeira, Bruna Ramos, Cynthia Costa, Marcos Romualdo Müller, Ulrich
author_sort	Gil-Sanz, Cristina
title	Proliferative Defects and Formation of a Double Cortex in Mice Lacking Mltt4 and Cdh2 in the Dorsal Telencephalon
title_short	Proliferative Defects and Formation of a Double Cortex in Mice Lacking Mltt4 and Cdh2 in the Dorsal Telencephalon
title_full	Proliferative Defects and Formation of a Double Cortex in Mice Lacking Mltt4 and Cdh2 in the Dorsal Telencephalon
title_fullStr	Proliferative Defects and Formation of a Double Cortex in Mice Lacking Mltt4 and Cdh2 in the Dorsal Telencephalon
title_full_unstemmed	Proliferative Defects and Formation of a Double Cortex in Mice Lacking Mltt4 and Cdh2 in the Dorsal Telencephalon
title_sort	proliferative defects and formation of a double cortex in mice lacking mltt4 and cdh2 in the dorsal telencephalon
publisher	The Journal of Neuroscience
publishDate	2014
url	https://repositorio.ufrn.br/jspui/handle/1/11823
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Proliferative Defects and Formation of a Double Cortex in Mice Lacking Mltt4 and Cdh2 in the Dorsal Telencephalon

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