Date of Award

2022

Department

Neuroscience

First Advisor

Dr. Helen Murphy

Abstract

Some mammalian species demonstrate the ability to regenerate functional photoreceptors after retinal injury, including those with mutations that result in non-syndromic diseases such as retinitis pigmentosa. Previous research has shown that regenerative capability exists in non-mutated animals following injury inflicted by light damage. Studies have suggested that, in mutated animals with inherited degeneration, regeneration does not occur spontaneously. However, mutated animals have exhibited regeneration following inflicted damage. Regenerative capabilities have been shown to be linked to the highly conserved Notch signaling pathway. To determine if differences in Notch signaling play a role in the lack of regeneration in zebrafish with inherited degeneration, Notch3 expression in a line of eys-/- zebrafish was quantified in relation to an unaffected heterozygous eys+/- zebrafish line, and a heterozygous line with inflicted light damage. Additionally, Notch3 expression in a line of Tg(XOPS:ntr-YFP) YFP+ zebrafish treated with metronidazole was quantified to compare regeneration capabilities of a chemical ablation damage model to those of the unaffected and light-damaged heterozygrous lines. Quantification results indicate that Notch3 expression is not upregulated in zebrafish with inherited degeneration in the way that it is in zebrafish with inflicted degeneration. Notch3 expression is downregulated in the chemical ablation model. The results are corroborated by investigation of proliferating cell counts in each group.

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