Cortex folding by combined progenitor expansion and adhesion-controlled neuronal migration

Folding of the mammalian cerebral cortex into sulcal fissures and gyral peaks is the result of complex processes that are incompletely understood. Previously we showed that genetic deletion of Flrt1/3 adhesion molecules causes folding of the smooth mouse cortex into sulci resulting from increased la...

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Detalles Bibliográficos
Autores: Chun, Seung Hee, Yoon, Da Eun, Diaz Almeida, Daniel Santiago, Todorov, Mihail Ivilinov, Straub, Tobias, Ruff, Tobias, Shao, Wei, Yang, Jianjun, Seyit Bremer, Gönül, Shen, Yi-Ru, Ertürk, Ali, Toro Ruiz, Daniel del, Shi, Songhai, Klein, Rüdiger
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2025
País:España
Institución:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:dnet:recercat____::ab039f2246d7e895f781a6212a21af11
Acceso en línea:https://hdl.handle.net/2445/228537
Access Level:acceso abierto
Palabra clave:Escorça cerebral
Evolució del cervell
Neurogenètica
Cerebral cortex
Evolution of the brain
Neurogenetics
Descripción
Sumario:Folding of the mammalian cerebral cortex into sulcal fissures and gyral peaks is the result of complex processes that are incompletely understood. Previously we showed that genetic deletion of Flrt1/3 adhesion molecules causes folding of the smooth mouse cortex into sulci resulting from increased lateral dispersion and faster neuron migration, without progenitor expansion. Here, we show in mice that combining the Flrt1/3 double knockout with an additional genetic deletion that causes progenitor expansion, greatly enhances cortex folding. Expansion of intermediate progenitors by deletion of Cep83 leads to a relative increase in Flrt-mutant neurons resulting in enhanced formation of sulci. Expansion of apical progenitors by deletion of Fgf10 leads to a relative reduction in Flrt-mutant neurons resulting in enhanced formation of gyri. These results together with computational modeling identify key developmental mechanisms, such as adhesive properties, cell densities and migration of cortical neurons, that cooperate to promote cortical gyrification.