Foxp1 Regulates Neural Stem Cell Self-Renewal and Bias Toward Deep Layer Cortical Fates.

Publication date: Feb 11, 2020

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 in maintaining 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-renewing cell 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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Pearson, C.A., Moore, D.M., Tucker, H.O., Dekker, J.D., Hu, H., Miquelaj’auregui, A., and Novitch, B.G. Foxp1 Regulates Neural Stem Cell Self-Renewal and Bias Toward Deep Layer Cortical Fates. 15226. 2020 Cell Rep (30):6.

Concepts Keywords
Autism FOXP1
Basal Radial glial cell
BRG Neurogenesis
Cortex Cerebral cortex
Cortical Stem cells
Embryogenesis Developmental neuroscience
Laminar Branches of biology
MRNA Critical autism
Neocortex Neuron
Neurogenesis
Neurogenic
Neuron
Postnatal
Protein
Radial Glia

Semantics

Type Source Name
drug DRUGBANK L-Arginine
disease MESH autism
disease MESH development
disease MESH autism spectrum disorder

Original Article

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