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An Intrinsic Epigenetic Barrier for Functional Axon Regeneration.

Neuron | Apr 19, 2017

Mature neurons in the adult peripheral nervous system can effectively switch from a dormant state with little axonal growth to robust axon regeneration upon injury. The mechanisms by which injury unlocks mature neurons' intrinsic axonal growth competence are not well understood. Here, we show that peripheral sciatic nerve lesion in adult mice leads to elevated levels of Tet3 and 5-hydroxylmethylcytosine in dorsal root ganglion (DRG) neurons. Functionally, Tet3 is required for robust axon regeneration of DRG neurons and behavioral recovery. Mechanistically, peripheral nerve injury induces DNA demethylation and upregulation of multiple regeneration-associated genes in a Tet3- and thymine DNA glycosylase-dependent fashion in DRG neurons. In addition, Pten deletion-induced axon regeneration of retinal ganglion neurons in the adult CNS is attenuated upon Tet1 knockdown. Together, our study suggests an epigenetic barrier that can be removed by active DNA demethylation to permit axon regeneration in the adult mammalian nervous system.

Pubmed ID: 28426967 RIS Download

Mesh terms: 5-Methylcytosine | Animals | Axons | Epigenesis, Genetic | Ganglia, Spinal | Mice, Inbred C57BL | Nerve Regeneration | Peripheral Nerve Injuries

Data used in this publication

None found

Associated grants

  • Agency: NINDS NIH HHS, Id: P01 NS097206
  • Agency: NINDS NIH HHS, Id: R35 NS097370
  • Agency: NIGMS NIH HHS, Id: T32 GM007814
  • Agency: NINDS NIH HHS, Id: R37 NS047344
  • Agency: NCI NIH HHS, Id: R01 CA078412
  • Agency: NCI NIH HHS, Id: P30 CA006927
  • Agency: NCI NIH HHS, Id: R01 CA160965

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