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Dryad

Notch directs telencephalic development and neuron fate determination by regulating miRNA levels

Abstract

The central nervous system (CNS) contains myriads of different types of cells produced from multipotent neural progenitors through multiple rounds of cell divisions. Neural progenitors acquire distinct cell identities depending on their spatial position, but they are also influenced by temporal cues to give rise to different cell populations over time. For instance, the progenitors of the cerebral neocortex generate different populations of excitatory projection neurons following a well-known sequence that is conserved across species. The Notch signaling pathway plays crucial roles in CNS development, including regulating the balance between proliferation and differentiation and fate acquisition. However, the molecular mechanisms by which Notch impacts progenitor fate decisions and telencephalic patterning have not been fully resolved. Here, we show that Notch signaling is essential for neocortical and hippocampal morphogenesis as well as for the development of the corpus callosum and the choroid plexus. In the neocortex, Notch regulates neural progenitor cell cycle dynamics, neurogenesis, and the laminar cytoarchitecture. Our data also indicate that Notch controls projection neuron fate determination through the regulation of two microRNA (miRNA) clusters that include let-7, miR-99a/100, and miR-125b. The expression of competitive inhibitors of these miRNAs rescues the effects of Notch gain-of-function in vivo. Our findings collectively suggest that balanced Notch signaling is crucial for telencephalic development and that the interplay between Notch and miRNAs is critical to control neocortical progenitor behaviors and neuron cell fate decisions.