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Activation of postnatal neural stem cells requires nuclear receptor TLX.

Neural stem cells (NSCs) continually produce new neurons in postnatal brains. However, the majority of these cells stay in a nondividing, inactive state. The molecular mechanism that is required for these cells to enter proliferation still remains largely unknown. Here, we show that nuclear receptor TLX (NR2E1) controls the activation status of postnatal NSCs in mice. Lineage tracing indicates that TLX-expressing cells give rise to both activated and inactive postnatal NSCs. Surprisingly, loss of TLX function does not result in spontaneous glial differentiation, but rather leads to a precipitous age-dependent increase of inactive cells with marker expression and radial morphology for NSCs. These inactive cells are mispositioned throughout the granular cell layer of the dentate gyrus during development and can proliferate again after reintroduction of ectopic TLX. RNA-seq analysis of sorted NSCs revealed a TLX-dependent global expression signature, which includes the p53 signaling pathway. TLX regulates p21 expression in a p53-dependent manner, and acute removal of p53 can rescue the proliferation defect of TLX-null NSCs in culture. Together, these findings suggest that TLX acts as an essential regulator that ensures the proliferative ability of postnatal NSCs by controlling their activation through genetic interaction with p53 and other signaling pathways.

Pubmed ID: 21957244


  • Niu W
  • Zou Y
  • Shen C
  • Zhang CL


The Journal of neuroscience : the official journal of the Society for Neuroscience

Publication Data

September 28, 2011

Associated Grants

  • Agency: NIH HHS, Id: 1DP2OD006484
  • Agency: NIH HHS, Id: DP2 OD006484
  • Agency: NIH HHS, Id: DP2 OD006484-01
  • Agency: NINDS NIH HHS, Id: R01 NS070981
  • Agency: NINDS NIH HHS, Id: R01 NS070981-01A1
  • Agency: NINDS NIH HHS, Id: R01NS070981

Mesh Terms

  • Animals
  • Animals, Newborn
  • Cell Proliferation
  • Cells, Cultured
  • HEK293 Cells
  • Humans
  • Mice
  • Mice, 129 Strain
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, Transgenic
  • Neural Stem Cells
  • Neurogenesis
  • Receptors, Cytoplasmic and Nuclear
  • Signal Transduction