Neural progenitors within the cerebral cortex undergo a characteristic switch between symmetric self-renewing cell divisions early in development and asymmetric neurogenic divisions at later times, yet the mechanisms controlling this transition remain unclear. Previous work has shown that the autism-linked transcription factor Foxp1 is endogenously expressed by early but not late neural progenitors, and both loss and gain of Foxp1 can alter neural progenitor activities and fate choices. Here, we show that early Foxp1 loss leads to an increase in transcriptional programs regulating angiogenesis, glycolysis, and cellular responses to hypoxia. These changes coincide with an elevation in Vegfa expression and precocious vascular network development. Thus, the endogenous decline in Foxp1 expression appears to orchestrate changes in the tissue environment adjacent to neural progenitors that influence their metabolic state which in turn can alter their self-renewal and neurogenic capacities.
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