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Neural stem cells, which exhibit self-renewal and multipotentiality, are generated in early embryonic brains and maintained throughout the lifespan. The mechanisms of their generation and maintenance are largely unknown. Here, we show that neural stem cells are generated independent of RBP-Jkappa, a key molecule in Notch signaling, by using RBP-Jkappa(-/-) embryonic stem cells in an embryonic stem cell-derived neurosphere assay. However, Notch pathway molecules are essential for the maintenance of neural stem cells; they are depleted in the early embryonic brains of RBP-Jkappa(-/-) or Notch1(-/-) mice. Neural stem cells also are depleted in embryonic brains deficient for the presenilin1 (PS1) gene, a key regulator in Notch signaling, and are reduced in PS1(+/-) adult brains. Both neuronal and glial differentiation in vitro were enhanced by attenuation of Notch signaling and suppressed by expressing an active form of Notch1. These data are consistent with a role for Notch signaling in the maintenance of the neural stem cell, and inconsistent with a role in a neuronal/glial fate switch.

Original publication

DOI

10.1101/gad.975202

Type

Journal article

Journal

Genes Dev

Publication Date

01/04/2002

Volume

16

Pages

846 - 858

Keywords

Animals, Brain, Bromodeoxyuridine, Cell Cycle, Cell Differentiation, Central Nervous System, Immunohistochemistry, Membrane Proteins, Mice, Microscopy, Fluorescence, Mutation, Neurons, Presenilin-1, Prosencephalon, Protein Binding, Receptor, Notch1, Receptors, Cell Surface, Receptors, Notch, Retroviridae, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, Time Factors, Transcription Factors