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Prdm16 regulates the postnatal fate of embryonic radial glia via Vcam1-dependent mechanisms

Author

Listed:
  • Jiwen Li

    (David Geffen School of Medicine at the University of California, Los Angeles (UCLA))

  • Marlesa I. Godoy

    (David Geffen School of Medicine at the University of California, Los Angeles (UCLA))

  • Yi Lu

    (David Geffen School of Medicine at the University of California, Los Angeles (UCLA))

  • Alice J. Zhang

    (David Geffen School of Medicine at the University of California, Los Angeles (UCLA))

  • Graciel Diamante

    (UCLA)

  • Elle Rathbun

    (UCLA)

  • Min Tian

    (UCLA)

  • In Sook Ahn

    (UCLA)

  • Arantxa Cebrian-Silla

    (University of California, San Francisco)

  • Arturo Alvarez-Buylla

    (University of California, San Francisco)

  • Xia Yang

    (UCLA
    Brain Research Institute at UCLA
    Institute for Quantitative and Computational Biosciences at UCLA
    Molecular Biology Institute at UCLA)

  • Bennett G. Novitch

    (Brain Research Institute at UCLA
    Molecular Biology Institute at UCLA
    UCLA
    Intellectual and Developmental Disabilities Research Center at UCLA)

  • S. Thomas Carmichael

    (UCLA
    Brain Research Institute at UCLA
    Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA)

  • Ye Zhang

    (David Geffen School of Medicine at the University of California, Los Angeles (UCLA)
    Brain Research Institute at UCLA
    Molecular Biology Institute at UCLA
    Intellectual and Developmental Disabilities Research Center at UCLA)

Abstract

The mammalian brain undergoes rapid and extensive neurogenesis during the embryonic stage and limited neurogenesis during the adult stage, which results in ineffective repair of neural circuits in adults. Currently, the molecular mechanisms regulating the postnatal termination of neurogenesis and the disappearance of embryonic radial glia, the neural stem cells (NSCs) responsible for neurogenesis, are largely unknown. Here, we show that genetic deletion of PR domain-containing 16 (Prdm16) from NSCs leads to the retention of radial glia in adulthood and prolonged postnatal neuroblast production. Mechanistically, Prdm16 induces a postnatal reduction in Vascular Cell Adhesion Molecule 1 (Vcam1). The extended presence of radial glia and neurogenesis phenotype is rescued in Prdm16-Vcam1 double knockout mice. These findings demonstrate that the inhibition of Vcam1 by Prdm16 promotes the postnatal cessation of neurogenesis and the disappearance of embryonic radial glia and provide valuable insights for regenerative medicine aimed at treating central nervous system disorders.

Suggested Citation

  • Jiwen Li & Marlesa I. Godoy & Yi Lu & Alice J. Zhang & Graciel Diamante & Elle Rathbun & Min Tian & In Sook Ahn & Arantxa Cebrian-Silla & Arturo Alvarez-Buylla & Xia Yang & Bennett G. Novitch & S. Tho, 2025. "Prdm16 regulates the postnatal fate of embryonic radial glia via Vcam1-dependent mechanisms," Nature Communications, Nature, vol. 16(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:16:y:2025:i:1:d:10.1038_s41467-025-60895-y
    DOI: 10.1038/s41467-025-60895-y
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