Developmentally upregulated transcriptional elongation factor a like 3 suppresses axon regeneration after optic nerve injury

Projection neurons of the mammalian central nervous system (CNS) do not spontaneously regenerate axons which have been damaged by an injury or disease, often leaving patients with permanent disabilities that affect motor, cognitive, or sensory functions. Although several molecular targets which promote some extent of axon regeneration in animal models have been identified, the resulting recovery is very limited, and the molecular mechanisms underlying the axonal regenerative failure in the CNS are still poorly understood. One of the most studied targets for axon regeneration in the CNS is the mTOR pathway. A number of developmentally regulated genes also have been found to play a role in CNS axon regeneration. Here, we found that Transcriptional Elongation Factor A Like 3 (Tceal3), belonging to the Bex/Tceal transcriptional regulator family, which also modulates the mTOR pathway, is developmentally upregulated in retinal ganglion cell (RGCs) projection CNS neurons, and suppresses their capacity to regenerate axons after injury.

Automated summary

Several molecular targets have been identified in animal models to promote axon regeneration in the central nervous system, but the resulting recovery is limited, and the mechanisms underlying axonal regenerative failure in the CNS are still poorly understood. Developmentally regulated genes and proteins that modulate the mTOR pathway have been found to play a role in CNS axon regeneration.