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The mTORC1 effectors S6K1 and 4E-BP play different roles in CNS axon regeneration

Author

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  • Liu Yang

    (Shriners Hospitals Pediatric Research Center (Center for Neural Repair and Rehabilitation), Temple University School of Medicine)

  • Linqing Miao

    (Shriners Hospitals Pediatric Research Center (Center for Neural Repair and Rehabilitation), Temple University School of Medicine)

  • Feisi Liang

    (Shriners Hospitals Pediatric Research Center (Center for Neural Repair and Rehabilitation), Temple University School of Medicine)

  • Haoliang Huang

    (Shriners Hospitals Pediatric Research Center (Center for Neural Repair and Rehabilitation), Temple University School of Medicine)

  • Xiuyin Teng

    (Shriners Hospitals Pediatric Research Center (Center for Neural Repair and Rehabilitation), Temple University School of Medicine)

  • Shaohua Li

    (Shriners Hospitals Pediatric Research Center (Center for Neural Repair and Rehabilitation), Temple University School of Medicine
    Union Hospital, Tongji Medical College, Huazhong University of Science and Technology)

  • Jaloliddin Nuriddinov

    (College of Science and Technology, Temple University)

  • Michael E. Selzer

    (Shriners Hospitals Pediatric Research Center (Center for Neural Repair and Rehabilitation), Temple University School of Medicine
    Temple University School of Medicine)

  • Yang Hu

    (Shriners Hospitals Pediatric Research Center (Center for Neural Repair and Rehabilitation), Temple University School of Medicine)

Abstract

Using mouse optic nerve (ON) crush as a CNS injury model, we and others have found that activation of the mammalian target of rapamycin complex 1 (mTORC1) in mature retinal ganglion cells by deletion of the negative regulators, phosphatase and tensin homologue (PTEN), and tuberous sclerosis 1 promotes ON regeneration. mTORC1 activation inhibits eukaryotic translation initiation factor 4E-binding protein (4E-BP) and activates ribosomal protein S6 kinase 1 (S6K1), both of which stimulate translation. We reasoned that mTORC1’s regeneration-promoting effects might be separable from its deleterious effects by differential manipulation of its downstream effectors. Here we show that S6K1 activation, but not 4E-BP inhibition, is sufficient to promote axon regeneration. However, inhibition of 4E-BP is required for PTEN deletion-induced axon regeneration. Both activation and inhibition of S6K1 decrease the effect of PTEN deletion on axon regeneration, implicating a dual role of S6K1 in regulating axon growth.

Suggested Citation

  • Liu Yang & Linqing Miao & Feisi Liang & Haoliang Huang & Xiuyin Teng & Shaohua Li & Jaloliddin Nuriddinov & Michael E. Selzer & Yang Hu, 2014. "The mTORC1 effectors S6K1 and 4E-BP play different roles in CNS axon regeneration," Nature Communications, Nature, vol. 5(1), pages 1-7, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms6416
    DOI: 10.1038/ncomms6416
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    1. Kai Zhou & Wei Wei & Dan Yang & Hui Zhang & Wei Yang & Yunpeng Zhang & Yingnan Nie & Mingming Hao & Pengcheng Wang & Hang Ruan & Ting Zhang & Shouyan Wang & Yaobo Liu, 2024. "Dual electrical stimulation at spinal-muscular interface reconstructs spinal sensorimotor circuits after spinal cord injury," Nature Communications, Nature, vol. 15(1), pages 1-26, December.

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