An essential role for a MEK-C/EBP pathway during growth factor-regulated cortical neurogenesis
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Updated: Sep 28, 2026

Rapid Detection of Neurodevelopmental Phenotypes in Human Neural Precursor Cells (NPCs)
Published on: March 2, 2018
Catherine Ménard1, Paul Hein, Annie Paquin
1Centre for Neuronal Survival and Brain Tumor Research Centre, Montreal Neurological Institute, Montreal, Canada.
Abstract:
Mammalian neurogenesis is determined by an interplay between intrinsic genetic mechanisms and extrinsic cues such as growth factors. Here we have defined a signaling cascade, a MEK-C/EBP pathway, that is essential for cortical progenitor cells to become postmitotic neurons. Inhibition of MEK or of the C/EBP family of transcription factors inhibits neurogenesis while expression of a C/EBPbeta mutant that is a phosphorylation-mimic at a MEK-Rsk site enhances neurogenesis. C/EBP mediates this positive effect by direct transcriptional activation of neuron-specific genes such as Talpha1 alpha-tubulin. Conversely, inhibition of C/EBP-dependent transcription enhances CNTF-mediated generation of astrocytes from the same progenitor cells. Thus, activation of a MEK-C/EBP pathway enhances neurogenesis and inhibits gliogenesis, thereby providing a mechanism whereby growth factors can selectively bias progenitors to become neurons during development.
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