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CRISPRi-Mediated Treatment of Dominant Rhodopsin-Associated Retinitis Pigmentosa
Journal article   Peer reviewed

CRISPRi-Mediated Treatment of Dominant Rhodopsin-Associated Retinitis Pigmentosa

Erin R Burnight, Luke A Wiley, Nathaniel K Mullin, Malavika K Adur, Mallory J Lang, Cathryn M Cranston, Chunhua Jiao, Stephen R Russell, Elliot H Sohn, Ian C Han, …
CRISPR journal, Vol.6(6), pp.502-513
12/2023
DOI: 10.1089/crispr.2023.0039
PMCID: PMC11304754
PMID: 38108516
url
https://pmc.ncbi.nlm.nih.gov/articles/PMC11304754/pdf/crispr.2023.0039.pdfView
Open Access

Abstract

Rhodopsin ( ) mutations such as Pro23His are the leading cause of dominantly inherited retinitis pigmentosa in North America. As with other dominant retinal dystrophies, these mutations lead to production of a toxic protein product, and treatment will require knockdown of the mutant allele. The purpose of this study was to develop a CRISPR-Cas9-mediated transcriptional repression strategy using catalytically inactive Cas9 (dCas9) fused to the Krüppel-associated box (KRAB) transcriptional repressor domain. Using a reporter construct carrying green fluorescent protein (GFP) cloned downstream of the promoter fragment (nucleotides -1403 to +73), we demonstrate a ∼74-84% reduction in promoter activity in CRISPRi-treated versus plasmid-only controls. After subretinal transduction of human retinal explants and transgenic Pro23His mutant pigs, significant knockdown of rhodopsin protein was achieved. Suppression of mutant transgene was associated with a reduction in endoplasmic reticulum (ER) stress and apoptosis markers and preservation of photoreceptor cell layer thickness.
Alleles Animals CRISPR-Cas Systems - genetics Gene Editing Humans Retinitis Pigmentosa - genetics Retinitis Pigmentosa - therapy Rhodopsin - genetics Swine

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