Assessing the effect of neuronal LZK and DLK deletion on Axonal Sprouting after CNS Injury

The goal of this project is to understand the roles of Leucine Zipper-bearing Kinase (LZK) and Dual Leucine Zipper Kinase (DLK), a pair of conserved mitogen-activated protein kinase kinase kinases (MAP3Ks) involved in axonal repair after central nervous system (CNS)injury. CNS injury often leads to partial and even complete loss of function mainly due to the inability of neurons to repair themselves after injuries. This lack of regenerative capacity in the CNS can be attributed to both intrinsic and extrinsic factors. The regeneration of severed axons and the compensatory sprouting of uninjured axons are two forms of axonal repair after CNS injury. The two MAP3Ks are believed to work in concert to regulate responses after injury to axons in the mammalian CNS. Of the two homologues, DLK has been the only mammalian homologue shown to be involved in axon regeneration after peripheral or optic nerve injury. However, the role of DLK in axonal repair in the mammalian spinal cord is not known, let alone LZK. Teamed with an MD/PhD student in the lab, I pursued a project to understand the isolated roles of DLK and LZK in models of corticospinal axon and sprouting in order to better understand their individual function in axonal repair after injury. The results complement the ongoing projects in the lab for a thorough understanding of the two MAP3Ks in axonal repair in the mammalian spinal cord after injury