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PI3K–GSK3 signalling regulates mammalian axon regeneration by inducing the expression of Smad1

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  • Saijilafu

    (The Johns Hopkins University School of Medicine)

  • Eun-Mi Hur

    (The Johns Hopkins University School of Medicine
    Center for Neuroscience, Brain Science Institute, Korea Institute of Science and Technology)

  • Chang-Mei Liu

    (The Johns Hopkins University School of Medicine)

  • Zhongxian Jiao

    (The Johns Hopkins University School of Medicine)

  • Wen-Lin Xu

    (The Johns Hopkins University School of Medicine)

  • Feng-Quan Zhou

    (The Johns Hopkins University School of Medicine
    The Johns Hopkins University School of Medicine)

Abstract

In contrast to neurons in the central nervous system, mature neurons in the mammalian peripheral nervous system (PNS) can regenerate axons after injury, in part, by enhancing intrinsic growth competence. However, the signalling pathways that enhance the growth potential and induce spontaneous axon regeneration remain poorly understood. Here we reveal that phosphatidylinositol 3-kinase (PI3K) signalling is activated in response to peripheral axotomy and that PI3K pathway is required for sensory axon regeneration. Moreover, we show that glycogen synthase kinase 3 (GSK3), rather than mammalian target of rapamycin, mediates PI3K-dependent augmentation of the growth potential in the PNS. Furthermore, we show that PI3K–GSK3 signal is conveyed by the induction of a transcription factor Smad1 and that acute depletion of Smad1 in adult mice prevents axon regeneration in vivo. Together, these results suggest PI3K–GSK3–Smad1 signalling as a central module for promoting sensory axon regeneration in the mammalian nervous system.

Suggested Citation

  • Saijilafu & Eun-Mi Hur & Chang-Mei Liu & Zhongxian Jiao & Wen-Lin Xu & Feng-Quan Zhou, 2013. "PI3K–GSK3 signalling regulates mammalian axon regeneration by inducing the expression of Smad1," Nature Communications, Nature, vol. 4(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3690
    DOI: 10.1038/ncomms3690
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