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<p>Cyclin-dependent kinase 7 (Cdk7) is a unique Cdk that drives cell proliferation and gene transcription. While its involvement in dividing cells as a Cdk-activating kinase (CAK) is essential for cell cycle progression, its function during the differentiation of postmitotic cells remains to be elucidated. Here, we show that loss of Cdk7 in developing cortical neurons critically hampers neurite growth and leads to aberrant social behaviors. Mechanistically, transcriptomic analysis reveals that the lack of Cdk7 in cortical neurons results in the downregulation of numerous genes controlling neuronal morphology, including several key players in the Calcium-dependent Wnt5a pathway. Interestingly, supplementing Cdk7-cKO neurons with Wnt5a ligand partially mitigates the observed defects in neuritogenesis. Our work highlights the importance of transcriptional Cdks beyond cell cycle exit and underscores their critical importance for normal brain function.</p>

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Cdk7 promotes neuritogenesis in cortical neurons and contributes to social behavior in mice

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月19日

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  • Sébastien Verteneuil,
  • Laura Van Hees,
  • Jean-Marc Lassance,
  • Camille Lejon,
  • Tine D’aes,
  • Quentin Marlier,
  • Pascale Quatresooz,
  • Laurence Delacroix,
  • Laurent Nguyen,
  • Brigitte Malgrange,
  • Renaud Vandenbosch

摘要

Cyclin-dependent kinase 7 (Cdk7) is a unique Cdk that drives cell proliferation and gene transcription. While its involvement in dividing cells as a Cdk-activating kinase (CAK) is essential for cell cycle progression, its function during the differentiation of postmitotic cells remains to be elucidated. Here, we show that loss of Cdk7 in developing cortical neurons critically hampers neurite growth and leads to aberrant social behaviors. Mechanistically, transcriptomic analysis reveals that the lack of Cdk7 in cortical neurons results in the downregulation of numerous genes controlling neuronal morphology, including several key players in the Calcium-dependent Wnt5a pathway. Interestingly, supplementing Cdk7-cKO neurons with Wnt5a ligand partially mitigates the observed defects in neuritogenesis. Our work highlights the importance of transcriptional Cdks beyond cell cycle exit and underscores their critical importance for normal brain function.