Journal
DEVELOPMENTAL CELL
Volume 35, Issue 5, Pages 553-567Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2015.11.005
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Funding
- Robertson Investigator Award from New York Stem Cell Foundation
- Maryland Stem Cell Research Funding (MSCRF/TEDCO)
- Adrienne Helis Malvin Medical Research Foundation
- Max Planck Society
- North Rhine-Westphalian Ministry for Innovation, Science and Research [314-400 010 09]
- European Research Council [ERC-2012-StG 310489-tRNA-modi]
- EMBO Long-Term Fellowship [ALTF1291-2010]
- F.R.S.- F.N.R.S.
- Fonds Leon Fredericq
- Fondation Medicale Reine Elisabeth
- Fondation Simone et Pierre Clerdent
- Belgian Science Policy [P7/20]
- ARC [ARC11/16-01]
- WELBIO
- Marie Curie
- EMBO
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The cerebral cortex contains layers of neurons sequentially generated by distinct lineage-related progenitors. At the onset of corticogenesis, the first-born progenitors are apical progenitors (APs), whose asymmetric division gives birth directly to neurons. Later, they switch to indirect neurogenesis by generating intermediate progenitors (IPs), which give rise to projection neurons of all cortical layers. While a direct lineage relationship between APs and IPs has been established, the molecular mechanism that controls their transition remains elusive. Here we show that interfering with codon translation speed triggers ER stress and the unfolded protein response (UPR), further impairing the generation of IPs and leading to microcephaly. Moreover, we demonstrate that a progressive downregulation of UPR in cortical progenitors acts as a physiological signal to amplify IPs and promotes indirect neurogenesis. Thus, our findings reveal a contribution of UPR to cell fate acquisition during mammalian brain development.
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