Journal
NEURON
Volume 103, Issue 6, Pages 1096-+Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2019.06.027
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Funding
- Belgian FRS/FNRS
- European Research Council (ERC Adv grant GENDEVOCORTEX)
- FMRE
- Interuniversity Attraction Poles Program (IUAP)
- WELBIO Program of the Walloon Region
- AXA Research Fund
- Fondation ULB
- ERA-net Microkin''
- Vlaams Instituut voor Biotechnologie (VIB)
- Francis Crick Institute - Cancer Research UK [FC0010089]
- UK Medical Research Council [FC0010089]
- Wellcome Trust [FC0010089]
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During neurogenesis, progenitors switch from self-renewal to differentiation through the interplay of intrinsic and extrinsic cues, but how these are integrated remains poorly understood. Here, we combine whole-genome transcriptional and epigenetic analyses with in vivo functional studies to demonstrate that Bcl6, a transcriptional repressor previously reported to promote cortical neurogenesis, acts as a driver of the neurogenic transition through direct silencing of a selective repertoire of genes belonging to multiple extrinsic pathways promoting self-renewal, most strikingly the Wnt pathway. At the molecular level, Bcl6 represses its targets through Sirt1 recruitment followed by histone deacetylation. Our data identify a molecular logic by which a single cell-intrinsic factor represses multiple extrinsic pathways that favor self-renewal, thereby ensuring robustness of neuronal fate transition.
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