Neurons must last an entire lifetime, despite facing frequent risk of injury that could result in issues such as neurodegenerative disease. Therefore, it is important to understand how neurons respond to injury and what cellular pathways are at play. Neuronal injury and cellular responses are often modeled in Drosophila by using a laser to sever neurites. Soft axon injury is commonly studied in the lab and produces a subtle calcium response followed by an upregulation in microtubules eight hours later. We recently observed an alternate type of axon injury, termed explosion injury, which produces an immediate, massive increase in cytosolic calcium and microtubule plus ends. This great contrast in responses prompted us to study this alternate type of injury further. In this study I characterize the microtubule response to explosion injury. I establish the requirement of calcium for plus-end upregulation, and the role of the microtubule severing protein fidgetin in cutting microtubules to produce more plus ends. Finally, I show that calpain A is a calcium-activated protein that is required for plus-end upregulation as well.
