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Knockout of phosphatase and tensin homolog (PTEN −/− ) is neuroprotective and promotes axon regeneration in mature neurons. Elevation of mTOR activity in injured neurons has been proposed as the primary underlying mechanism. Here we demonstrate that PTEN −/−  also abrogates the inhibitory activity of GSK3 on collapsin response mediator protein 2 (CRMP2) in retinal ganglion cell (RGC) axons. Moreover, maintenance of GSK3 activity in  Gsk3   S/A   knockin mice significantly compromised PTEN −/− -mediated optic nerve regeneration as well as the activity of CRMP2, and to a lesser extent, mTOR. These GSK3 S/A  mediated negative effects on regeneration were rescued by viral expression of constitutively active CRMP2 T/A , despite decreased mTOR activation.  Gsk3   S/A   knockin or CRMP2 inhibition also decreased PTEN −/−  mediated neurite growth of RGCs in culture and disinhibition towards CNS myelin. Thus, the GSK3/CRMP2 pathway is essential for PTEN −/−  mediated axon regeneration. These new mechanistic insights may help to find novel strategies to promote axon regeneration.

GSK3-CRMP2 signaling mediates axonal regeneration induced by Pten knockout