Abstract
The capacity of an axon to regenerate is regulated by its external environment and by cell-intrinsic factors. Studies in a variety of organisms suggest that alterations in axonal microtubule (MT) dynamics have potent effects on axon regeneration. We review recent findings on the regulation of MT dynamics during axon regeneration, focusing on the nematode Caenorhabditis elegans. In C. elegans the dual leucine zipper kinase (DLK) promotes axon regeneration, whereas the exchange factor for Arf6 (EFA-6) inhibits axon regeneration. Both DLK and EFA-6 respond to injury and control axon regeneration in part via MT dynamics. How the DLK and EFA-6 pathways are related is a topic of active investigation, as is the mechanism by which EFA-6 responds to axonal injury. We evaluate potential candidates, such as the MT affinity-regulating kinase PAR-1/MARK, in regulation of EFA-6 and axonal MT dynamics in regeneration.
Highlights
More than a hundred years ago, Ramon y Cajal was the first to describe how individual axons respond to injury[1]
Both dual leucine zipper kinase (DLK) and exchange factor for Arf6 (EFA-6) respond to injury and control axon regeneration in part via MT dynamics
We evaluate potential candidates, such as the MT affinity-regulating kinase PAR-1/MARK, in regulation of EFA-6 and axonal MT dynamics in regeneration
Summary
More than a hundred years ago, Ramon y Cajal was the first to describe how individual axons respond to injury[1]. The roles of mammalian EFA6 family members in axon regeneration remain to be examined, Xenopus TACC3 promotes axon outgrowth in embryonic cultured neural crest cells[65], and DCLK is required in mammalian axon regrowth[66], suggesting potential functional conservation from C. elegans to mammals. Neurite outgrowth involves a pioneer population of dynamic MTs that invades growth cones, followed by MT stabilization in axon extension[74] These studies suggest that PAR-1/MARK plays key roles in MT plasticity during neurite outgrowth; less is known of its roles in axon regeneration. DLK-1 promotes MT dynamics and growth, whereas EFA-6 relocalizes close to the MT minus ends to inhibit MT dynamics Both proteins seem to affect axon regeneration by regulating MT dynamics. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
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