
Investigating the Proteins and Mechanisms Involved in Axon Regeneration after Injury
Neurons do not replicate, so they cannot be replaced if they are damaged by neurodegenerative disease, traumatic injury, stroke, etc. This means that the study of how neurons can repair vital structures like axons is very important. Peripheral neurons can regenerate their axons after injury, but central nervous system neurons cannot. The mechanism of peripheral nervous system axon regeneration is not fully understood, so my project focused on determining the proteins involved. Previous studies have shown that the smooth endoplasmic reticulum (ER) must accumulate at the tip of the regenerating axon or axon regeneration will be significantly reduced. I sought to understand why the smooth ER is necessary for axon regeneration by studying the smooth ER calcium channel, ryanodine receptor (RyR). I knocked down expression of RyR using RNAi and compared axon regeneration in knockdown larvae to normal larvae. I found that RyR knockdown significantly reduces axon regeneration after injury which suggests that calcium release from the smooth ER through RyR is involved in axon regeneration. I also tested how RyR knockdown impacts DLK pathway activation after injury and found that it does not significantly affect DLK pathway activation. This suggests that RyR might not be involved in axon regeneration initiation through the DLK pathway. As a whole, my results show that RyR is important for axon regeneration and likely acts somewhere downstream of axon regeneration initiation.
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Work Title | Investigating the Proteins and Mechanisms Involved in Axon Regeneration after Injury |
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License | No Copyright - U.S. |
Work Type | Research Paper |
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Publication Date | April 26, 2024 |
Deposited | April 26, 2024 |
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