Document Type

Poster

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Abstract

While mammals possess a limited capacity for retinal regeneration, teleosts such as Danio rerio (zebrafish) can recover from retinal injury or cell death through stimulation of glia to induce reprogramming into neural stem-like cells.

1 In zebrafish, retinal Müller glia engage in regeneration in response to an injury-derived signal. It was previously shown2,3 that the regenerative response to retinal damage in zebrafish is regulated by the Notch signaling pathway. Persistent Notch signaling causes Müller glia to remain in a quiescent state in the undamaged retina, and Notch signaling repression causes Müller glia to reenter the cell cycle3 , reprogramming them to stem-like cells that undergo division and produce multi-potent retinal progenitors, which are then able to exit the cell cycle and differentiate into replacements for the damaged neurons. There is evidence that Müller cells do not proliferate in the mutants studied with inherited photoreceptor degeneration, but they do proliferate after the retina is injured. 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.

Publication Date

Spring 2022

Comments

Advised by Dr. Helen Murphy and Dr. Cyrilla Wideman of the Neuroscience Program

Notch3 Expression in Zebrafish with Inherited Degeneration vs. Inflicted Damage

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