June 2022
Volume 63, Issue 7
Open Access
ARVO Annual Meeting Abstract  |   June 2022
Cas13 RNA base editing targeting stop mutation in ABCA4
Author Affiliations & Notes
  • Elena Piotter
    Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, Oxfordshire, United Kingdom
  • Michelle E. McClements
    Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, Oxfordshire, United Kingdom
  • Robert E MacLaren
    Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, Oxfordshire, United Kingdom
    Oxford Eye Hospital, Oxford, Oxfordshire, United Kingdom
  • Footnotes
    Commercial Relationships   Elena Piotter None; Michelle McClements None; Robert MacLaren None
  • Footnotes
    Support  Retina UK, Macula Society, NIHR Oxford Biomedical Research Centre
Investigative Ophthalmology & Visual Science June 2022, Vol.63, 82 – A0055. doi:
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    • Get Citation

      Elena Piotter, Michelle E. McClements, Robert E MacLaren; Cas13 RNA base editing targeting stop mutation in ABCA4. Invest. Ophthalmol. Vis. Sci. 2022;63(7):82 – A0055.

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

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Abstract

Purpose : Stargardt macular dystrophy (STGD1) is the most prevalent form of inherited macular dystrophy worldwide and is therefore highly clinically relevant. To date, a variety of gene supplementation approaches have been tested to create a therapy with some reaching clinical trials. Currently, however, no treatment exists. Newer technologies, such as RNA base editors, enable correction of pathogenic G>A and T>C mutation correction. ABCA4 has ~1200 known pathogenic mutations, of which ~63% are transition mutations amenable to this editing technology. Here, we investigated the use of a Cas13-ADAR RNA base editing system to correct an ABCA4 pathogenic stop mutation, c.206 G>A; p.W60*.

Methods : These experiments used a dual luciferase reporter assay comparing expression of Firefly luciferin to constitutively expressed Renilla luciferin. Fragments of the ABCA4 gene containing the desired mutation, c.206 G>A; p.W60* were inserted in-frame between the two luciferase elements with flanking F2A sites. As the insert contains a stop codon in frame, Firefly is not expressed but when mutation correction occurs, Firefly is expressed. The assay involved a triple transfection of HEK293T cells with the Cas13b-ADAR construct, the luciferase reporter plasmid, and the gRNA plasmid, for which 15 guide variants were tested. The output is the ratio of Firefly to Renilla expression.

Results : Initial findings indicate that all 15 guides show activity relative to the mutant plasmid and the non-targeting control (NTC), p<0.0001. Three guides showed statistically significant levels of editing, G6, G7, and G12, relative to the mutant plasmid. However, there was no significant difference between guides. When taken as a percentage of the wild-type (WT) plasmid ie no mutation, these guides showed between 28-34% of WT expression. Further, initial transcript analysis using EditR was performed, where 43-61% of transcripts showed the WT ‘G’ instead of an 'A' with guides 6, 7, and 12.

Conclusions : Overall, previous meta-analyses show 63% of pathogenic mutations in ABCA4 are amenable to Cas13b RNA base editing, particularly as there is no PAM-site constraint. This is a first look at RNA base editing targeting a mutation in ABCA4. The findings indicate that RNA base editing shows potential in targeting an ABCA4 sequence, thus indicating a clinical potential for Stargardt disease.

This abstract was presented at the 2022 ARVO Annual Meeting, held in Denver, CO, May 1-4, 2022, and virtually.

 

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