Investigative Ophthalmology & Visual Science Cover Image for Volume 65, Issue 7
June 2024
Volume 65, Issue 7
Open Access
ARVO Annual Meeting Abstract  |   June 2024
Gene Editing Based Rescue of Deep-Intronic Variants in Intron 30 of ABCA4-Associated with Severe Forms of Stargardt’s Disease
Author Affiliations & Notes
  • Poulami Chaudhuri
    Helex Inc, New York, New York, United States
  • Harsha Rohira
    Helex Inc, New York, New York, United States
  • Rakesh Kappagantu
    Helex Inc, New York, New York, United States
  • Anita Hoogendoorn
    Radboudumc, Nijmegen, Gelderland, Netherlands
  • Dyah W Karjosukarso
    Radboudumc, Nijmegen, Gelderland, Netherlands
  • Edwin M. van Oosten
    Radboudumc, Nijmegen, Gelderland, Netherlands
  • Rob Collin
    Radboudumc, Nijmegen, Gelderland, Netherlands
  • Alex Garanto
    Radboudumc, Nijmegen, Gelderland, Netherlands
  • Footnotes
    Commercial Relationships   Poulami Chaudhuri None; Harsha Rohira None; Rakesh Kappagantu None; Anita Hoogendoorn None; Dyah Karjosukarso None; Edwin M. van Oosten None; Rob Collin None; Alex Garanto None
  • Footnotes
    Support  none
Investigative Ophthalmology & Visual Science June 2024, Vol.65, 6067. doi:
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      Poulami Chaudhuri, Harsha Rohira, Rakesh Kappagantu, Anita Hoogendoorn, Dyah W Karjosukarso, Edwin M. van Oosten, Rob Collin, Alex Garanto; Gene Editing Based Rescue of Deep-Intronic Variants in Intron 30 of ABCA4-Associated with Severe Forms of Stargardt’s Disease. Invest. Ophthalmol. Vis. Sci. 2024;65(7):6067.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : STGD1 a rare form of macular degeneration, has a high unmet need and no approved treatment yet. The purpose is to (1) show the effect of the deep-intronic variant c.4539+2001 G>A in intron 30 of ABCA4 in patient derived cell models on ABCA4 protein (2) use gene editing to rescue the aberrant splicing and restore protein production as a proof of concept to create a potential single dose therapeutic for patients with deep-intronic variants in ABCA4.

Methods : The impact of deep-intronic mutations in intron 30 of ABCA4 was assessed based on observing aberrant transcripts by RT-PCR analysis in three compound heterozygous mutant STGD1 patient iPSC-derived RPE cells (c.4539+1106C>T, c.4539+2001G>A, c.4539+2028C>T) in comparison to healthy control RPE cells. Immunostaining of a patient-derived (c.4539+2001G>A, compound heterozygous) retinal organoid generated after 175 days of differentiation was performed to screen for ABCA4 protein localization. DAPI (blue) was used to stain the nuclei and anti-ABCA4 antibody was used to stain the ABCA4 protein.
Helex’s proprietary EPIC-Cure platform was used to design two gRNAs to excise a region in intron 30 that spans six mutations (c.4539+1100 A>G, c.4539+1106 C>T, c.4539+2001 G>A, c.4539+2028 C>T, c.4539+2064 C>T, and c.4539+2066 C>G). Patient derived fibroblasts (c.4539+2001 G>A) were transfected with gRNAs with Cas9 mRNA using Lipofectamine messenger max. Target-specific PCR amplification was performed on genomic DNA post transfection to estimate excision efficiency. Control and patient-derived cells were transdifferentiated for 10 days, treated with cycloheximide to block nonsense-mediated decay and RT-PCR was performed to check for aberrant transcripts.

Results : RT-PCR analysis of STGD1 patient-derived fibroblasts and immunostaining of the patient-derived organoids displayed formation of aberrant transcript and loss of correct ABCA4 protein localization confirming the pathogenicity of the specific deep-intronic mutations. High efficiency target region excision was observed with Helex’s proprietary gRNAs. RT-PCR analysis of the transdifferentiated heterogenous edited population demonstrated significant reduction in aberrant mRNA transcript.

Conclusions : Our work serves as a strong proof of concept to further develop a gene editing- based approach for patients with deep-intronic mutations in ABCA4 that lead to Stargardt disease.

This abstract was presented at the 2024 ARVO Annual Meeting, held in Seattle, WA, May 5-9, 2024.

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