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Teleost fish such as zebrafish (Danio rerio) have shown the ability to regenerate damaged photoreceptors due to the robust activity of Müller glia [1]. Interestingly, the Müller glia in retinal disease model zebrafish such as bbs2, cep290, and eys do not respond like those in normal zebrafish, making these genotypes a good model to study treatment options in humans [2, 3, 4]. The Notch signaling pathway is a highly conserved cell signaling pathway in many organisms that plays a role in determining cell fates in developmental processes [5]. Specifically, the notch3 gene has been studied and shown to have effects on Müller glia proliferation [6,7]. In the zebrafish retina, Notch signaling has been determined to be necessary to inhibit the differentiation and proliferation of Müller glia cells [6]. What is unknown is how retinal disease model zebrafish respond to Notch signaling targets. In the current study, the embryos of each disease model line (bbs2, cep290, and eys) were injected with two different CRISPRs separately, targeting exon 2 and exon 4 of the notch3 gene, and retinal tissue sections of 4–6-month-old zebrafish were stained for PCNA to quantify retinal regeneration.

Publication Date

Spring 2022


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

Targeting notch3 with CRISPR-Cas9 technology in zebrafish retinal degeneration models

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Neurosciences Commons