Characterizing Neuronal Response to Simultaneous Axon and Dendrite Injury in Drosophila

Open Access
Author:
Mandel, Jenna Lauren
Area of Honors:
Biology
Degree:
Bachelor of Science
Document Type:
Thesis
Thesis Supervisors:
  • Melissa Rolls, Thesis Supervisor
  • Richard Ordway , Honors Advisor
Keywords:
  • Neuron
  • Axon
  • Dendrites
  • Drosophila
  • Injury
  • Regeneration
Abstract:
Neurons are post-mitotic nerve cells that comprise both the central and peripheral nervous systems. They receive information via dendritic processes, and send information to neighboring cells by propagating signals down the axon. Without axons and dendrites, neurons cannot function properly. Neurons are incapable of being replaced in the event of cell death, so their ability to respond to injury is critical. Damage to both neuronal processes is likely to occur in response to stroke and traumatic brain injury. Although neurons have been shown to survive injury by regenerating damaged processes, simultaneous injury of both the axon and dendrite has rarely been performed or studied experimentally in vivo. Since neuronal survival is critical for humans, and simultaneous axon and dendrite damage is likely to occur in response to certain neurological diseases, it is crucial to understand the cellular mechanisms responsible for facilitating either the death or survival of these nerve cells. I aimed to characterize the neuronal response to simultaneous axon and dendrite injury, and to determine whether neurons are capable of regeneration following such severe damage. It has previously been shown that axons regenerate via activation of a conserved kinase cascade known as the Dual Leucine Zipper Kinase (DLK) pathway. Though dendrite regeneration has been shown to be rapid and robust, the mechanism by which dendrites regenerate is not yet known. I also sought to understand whether these pathways for regeneration are mutually exclusive when the need for both arises simultaneously. Our data indicate that neurons are capable of surviving complete ablation of their axons and dendrites and are, remarkably, able to regenerate both axons and dendrites in response to this severe injury. Investigating the mechanistic machinery that facilitates regenerative responses to various types of injury will be fundamental in aiding the reparation of damaged mammalian neurons. We demonstrate the ability of neurons to successfully regenerate axons and dendrites in response injury of both cellular processes. This has not been shown previously, so this finding has incredible potential to eventually help patients of stroke and traumatic brain injury.