Journal
CELL REPORTS
Volume 30, Issue 6, Pages 1964-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2020.01.034
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Funding
- UCLA Broad Stem Cell Research Center
- NIH [R01NS089817, R01NS085227, R01NS072804, R01AI059447, P20GM103642]
- California Institute for Regenerative Medicine [DISC1-08819]
- Cancer Prevention and Research Institute of Texas (CPRIT) [RP100612, RP120348]
- Marie Betzner Morrow Centennial Endowment
- UCLA-California Institute for Regenerative Medicine Training Grant [TG2-01169]
- Lymphoma Research Foundation [300463]
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The laminar architecture of the mammalian neocortex depends on the orderly generation of distinct neuronal subtypes by apical radial glia (aRG) during embryogenesis. Here, we identify critical roles for the autism risk gene Foxp1 inmaintaining aRG identity and gating the temporal competency for deep-layer neurogenesis. Early in development, aRG express high levels of Foxp1 mRNA and protein, which promote self-renewingcell divisions and deep-layer neuron production. Foxp1 levels subsequently decline during the transition to superficial-layer neurogenesis. Sustained Foxp1 expression impedes this transition, preserving a population of cells with aRG identity throughout development and extending the early neurogenic period into postnatal life. FOXP1 expression is further associated with the initial formation and expansion of basal RG (bRG) during human corticogenesis and can promote the formation of cells exhibiting characteristics of bRG when misexpressed in the mouse cortex. Together, these findings reveal broad functions for Foxp1 in cortical neurogenesis.
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