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Título: Proliferative Defects and Formation of a Double Cortex in Mice Lacking Mltt4 and Cdh2 in the Dorsal Telencephalon
Autor(es): Gil-Sanz, Cristina
Landeira, Bruna
Ramos, Cynthia
Costa, Marcos Romualdo
Müller, Ulrich
Palavras-chave: afadin;CDH2;double cortex;neocortex;progenitor;radial glia
Data do documento: 6-Ago-2014
Editor: The Journal of Neuroscience
Referência: 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.
Abstract: 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.
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