Cell cycle arrest determines adult neural stem cell ontogeny by an embryonic Notch-nonoscillatory Hey1 module

Nat Commun. 2021 Nov 12;12(1):6562. doi: 10.1038/s41467-021-26605-0.

Abstract

Quiescent neural stem cells (NSCs) in the adult mouse brain are the source of neurogenesis that regulates innate and adaptive behaviors. Adult NSCs in the subventricular zone are derived from a subpopulation of embryonic neural stem-progenitor cells (NPCs) that is characterized by a slower cell cycle relative to the more abundant rapid cycling NPCs that build the brain. Yet, how slow cell cycle can cause the establishment of adult NSCs remains largely unknown. Here, we demonstrate that Notch and an effector Hey1 form a module that is upregulated by cell cycle arrest in slowly dividing NPCs. In contrast to the oscillatory expression of the Notch effectors Hes1 and Hes5 in fast cycling progenitors, Hey1 displays a non-oscillatory stationary expression pattern and contributes to the long-term maintenance of NSCs. These findings reveal a novel division of labor in Notch effectors where cell cycle rate biases effector selection and cell fate.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult Stem Cells / metabolism*
  • Animals
  • Basic Helix-Loop-Helix Transcription Factors / metabolism
  • Brain / cytology
  • Cell Cycle / genetics
  • Cell Cycle / physiology
  • Cell Cycle Checkpoints / genetics
  • Cell Cycle Checkpoints / physiology*
  • Cell Cycle Proteins / genetics
  • Cell Cycle Proteins / metabolism*
  • Embryonic Stem Cells
  • Gene Expression
  • Lateral Ventricles / metabolism
  • Mice
  • Nervous System
  • Neurogenesis / genetics
  • Neurogenesis / physiology*
  • Receptor, Notch1
  • Repressor Proteins / metabolism

Substances

  • Basic Helix-Loop-Helix Transcription Factors
  • Cell Cycle Proteins
  • Hes5 protein, mouse
  • Hey1 protein, mouse
  • Notch1 protein, mouse
  • Receptor, Notch1
  • Repressor Proteins