PI3K-GSK3 signalling regulates mammalian axon regeneration by inducing the expression of Smad1
- PI3K-GSK3 signalling regulates mammalian axon regeneration by inducing the expression of Smad1
- Saijilafu; 허은미; Chang-Mei Liu; Zhongxian Jiao; Wen-Lin Xu; Feng-Quan Zhou
- Biological sciences; Cell biology; Neuroscience
- Issue Date
- Nature Communications
- VOL 4, 2690-1-2690-14
- 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.
- Appears in Collections:
- KIST Publication > Article
- Files in This Item:
There are no files associated with this item.
- RIS (EndNote)
- XLS (Excel)
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.