Abstract
Axon regeneration after injury is a conserved biological process that involves a large number of molecular pathways, including rapid calcium influx at injury sites, retrograde injury signaling, epigenetic transition, transcriptional reprogramming, polarized transport, and cytoskeleton reorganization. Despite the numerous efforts devoted to understanding the underlying cellular and molecular mechanisms of axon regeneration, the search continues for effective target molecules for improving axon regeneration. Although there have been significant historical efforts towards characterizing pro-regenerative factors involved in axon regeneration, the pursuit of intrinsic inhibitors is relatively recent. EFA6 (exchange factor for ARF6) has been demonstrated to inhibit axon regeneration in different organisms. EFA6 inhibition could be a promising therapeutic strategy to promote axon regeneration and functional recovery after axon injury. This review summarizes the inhibitory role on axon regeneration through regulating microtubule dynamics and through affecting ARF6 (ADP-ribosylation factor 6) GTPase-mediated integrin transport.
Highlights
In the adult mammalian central nervous system (CNS), injured axons have a very limited regeneration capacity, resulting in the failure of functional recovery after trauma [1]. This is fundamentally different in the peripheral nervous system (PNS) and in the embryonic CNS, where axons display strong regeneration after injury [2]
To examine whether EFA-6 regulates axonal microtubules, we examined microtubule dynamics marked by the plus end binding protein EBP-2 [20,74]
EFA6 is a conserved protein that is known to act as a GEF for ARF6 GTPase
Summary
In the adult mammalian central nervous system (CNS), injured axons have a very limited regeneration capacity, resulting in the failure of functional recovery after trauma [1]. Laser assisted axotomies have been utilized in combination with extensive genetic and drug screenings to identify the expression pathways involved in regulating axon regeneration from a traumatic injury [20,21,22]. Within these genetic screens, EFA6 (exchange factor for ARF6) was identified as a negative regulator of axon regrowth [20]. Given the inhibitory role of EFA6 in axon regeneration, we suggest that inhibition of EFA6 could be a promising strategy to promote axon regeneration
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