RAB6 and dynein drive post-Golgi apical transport to prevent neuronal progenitor delamination

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Brault, Jean‐baptiste | Bardin, Sabine | Lampic, Marusa | Carpentieri, Jacopo, A | Coquand, Laure | Penisson, Maxime | Lachuer, Hugo | Victoria, Guiliana, Soraya | Baloul, Sarah | El Marjou, Fatima | Boncompain, Gaelle | Miserey‐lenkei, Stephanie | Belvindrah, Richard | Fraisier, Vincent | Francis, Fiona | Perez, Franck | Goud, Bruno | Baffet, Alexandre, D

Edité par CCSD ; EMBO Press -

International audience. Radial glial (RG) cells are the neural stem cells of the developing neocortex. Apical RG (aRG) cells can delaminate to generate basal RG (bRG) cells, a cell type associated with human brain expansion. Here, we report that aRG delamination is regulated by the post-Golgi secretory pathway. Using in situ subcellular live imaging, we show that post-Golgi transport of RAB6+ vesicles occurs toward the minus ends of microtubules and depends on dynein. We demonstrate that the apical determinant Crumbs3 (CRB3) is also transported by dynein. Double knockout of RAB6A/A' and RAB6B impairs apical localization of CRB3 and induces a retraction of aRG cell apical process, leading to delamination and ectopic division. These defects are phenocopied by knockout of the dynein activator LIS1. Overall, our results identify a RAB6-dynein-LIS1 complex for Golgi to apical surface transport in aRG cells, and highlights the role of this pathway in the maintenance of neuroepithelial integrity.

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