| Literature DB >> 26651292 |
Sophie Laguesse1, Catherine Creppe1, Danny D Nedialkova2, Pierre-Paul Prévot1, Laurence Borgs1, Sandra Huysseune1, Bénédicte Franco1, Guérin Duysens1, Nathalie Krusy1, Gabsang Lee3, Nicolas Thelen1, Marc Thiry1, Pierre Close4, Alain Chariot5, Brigitte Malgrange1, Sebastian A Leidel6, Juliette D Godin7, Laurent Nguyen8.
Abstract
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.Entities:
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Year: 2015 PMID: 26651292 DOI: 10.1016/j.devcel.2015.11.005
Source DB: PubMed Journal: Dev Cell ISSN: 1534-5807 Impact factor: 12.270