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RAB6 and dynein drive post‐Golgi apical transport to prevent neuronal progenitor delamination
Author(s) -
Brault JeanBaptiste,
Bardin Sabine,
Lampic Marusa,
Carpentieri Jacopo A,
Coquand Laure,
Penisson Maxime,
Lachuer Hugo,
Victoria Guiliana Soraya,
Baloul Sarah,
El Marjou Fatima,
Boncompain Gaelle,
MisereyLenkei Stephanie,
Belvindrah Richard,
Fraisier Vincent,
Francis Fiona,
Perez Franck,
Goud Bruno,
Baffet Alexandre D
Publication year - 2022
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.202254605
Subject(s) - microbiology and biotechnology , golgi apparatus , dynein , microtubule , progenitor cell , axoplasmic transport , biology , chemistry , endoplasmic reticulum , stem cell
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.