Dual Threat: DLK as a Novel Role Player in Axonal Regeneration

by Aaron Gochman (’18)

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Fig. 1: Scientists have discovered a previously unknown role for Dual-leucine zipper kinase, an activating enzyme found in neurons.

Axonal regeneration is a branch of neuroscience on the cutting edge; re-growing injured neurons is a technique that, once refined, will fundamentally change the landscape of nervous system therapies. A team of researchers from University of Michigan, Washington University in St. Louis, and University of Pennsylvania have discovered a key intracellular pathway in axonal regeneration that is conserved in both Drosophila, more commonly known as fruit flies, and mammalian neurons.

The researchers characterized a mechanism called Dual Leucine-zipper kinase (DLK), which is critical in the activation of cAMP, a known effector molecule in axonal regrowth processes. The means by which cAMP is stimulated to induce regeneration have been unknown, but the linkage with DLK offers a clue to its biological mechanism. DLK is phosphorylated by protein kinase A (PKA), after which it interacts with cAMP.

Although DLK is considered the “injury sensor” because it is known to be active after injury, both PKA and DLK are crucial in the proper functioning of cAMP, the molecule that ultimately affects axonal regrowth. These findings are important because they offer a new clue to the pathway by which neurons heal from injury; once these fundamental processes are understood, they present a new avenue that can be targeted with therapy.  

References:

  1. Y. Hao, et. al., An evolutionarily conserved mechanism for cAMP elicited axonal regeneration involves direct activation of the dual leucine zipper kinase DLK. eLife, 5, (2016), doi: http://dx.doi.org/10.7554/eLife.14048

  2. “Untangling Neurons.” National Institutes of Health. U.S. Department of Health and Human Services, 2016 20 Apr. Web.

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