Double-strand break repair pathways differentially affect processing and transduction by dual AAV vectors

Abstract Recombinant adeno-associated viral vectors (rAAV) are a powerful tool for gene delivery but have a limited DNA carrying capacity. Efforts to expand this genetic payload have focused on engineering the vector components, such as dual trans-splicing vectors which double the delivery size by e...

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Main Authors: Anna C. Maurer, Brian Benyamini, Oscar N. Whitney, Vinson B. Fan, Claudia Cattoglio, Djem U. Kissiov, Gina M. Dailey, Xavier Darzacq, Matthew D. Weitzman, Robert Tjian
Format: Article
Language:English
Published: Nature Portfolio 2025-02-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-56738-5
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author Anna C. Maurer
Brian Benyamini
Oscar N. Whitney
Vinson B. Fan
Claudia Cattoglio
Djem U. Kissiov
Gina M. Dailey
Xavier Darzacq
Matthew D. Weitzman
Robert Tjian
author_facet Anna C. Maurer
Brian Benyamini
Oscar N. Whitney
Vinson B. Fan
Claudia Cattoglio
Djem U. Kissiov
Gina M. Dailey
Xavier Darzacq
Matthew D. Weitzman
Robert Tjian
author_sort Anna C. Maurer
collection DOAJ
description Abstract Recombinant adeno-associated viral vectors (rAAV) are a powerful tool for gene delivery but have a limited DNA carrying capacity. Efforts to expand this genetic payload have focused on engineering the vector components, such as dual trans-splicing vectors which double the delivery size by exploiting the natural concatenation of rAAV genomes in host nuclei. We hypothesized that inefficient dual vector transduction could be improved by modulating host factors which affect concatenation. Since factors mediating concatenation are not well defined, we performed a genome-wide screen to identify host cell regulators. We discover that Homologous Recombination (HR) is inhibitory to dual vector transduction. We demonstrate that depletion or inhibition of HR factors BRCA1 and Rad51 significantly increase reconstitution of a large split transgene by increasing both concatenation and expression from rAAVs. Our results define roles for DNA damage repair in rAAV transduction and highlight the potential for pharmacological intervention to increase genetic payload of rAAV vectors.
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spelling doaj-art-efbba43e125e40ec8bf6ba10728fdc5c2025-08-20T02:13:02ZengNature PortfolioNature Communications2041-17232025-02-0116111410.1038/s41467-025-56738-5Double-strand break repair pathways differentially affect processing and transduction by dual AAV vectorsAnna C. Maurer0Brian Benyamini1Oscar N. Whitney2Vinson B. Fan3Claudia Cattoglio4Djem U. Kissiov5Gina M. Dailey6Xavier Darzacq7Matthew D. Weitzman8Robert Tjian9Department of Molecular and Cell Biology, University of CaliforniaDepartment of Molecular and Cell Biology, University of CaliforniaDepartment of Molecular and Cell Biology, University of CaliforniaDepartment of Molecular and Cell Biology, University of CaliforniaDepartment of Molecular and Cell Biology, University of CaliforniaDepartment of Molecular and Cell Biology, University of CaliforniaDepartment of Molecular and Cell Biology, University of CaliforniaDepartment of Molecular and Cell Biology, University of CaliforniaDepartment of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine and the Children’s Hospital of PhiladelphiaDepartment of Molecular and Cell Biology, University of CaliforniaAbstract Recombinant adeno-associated viral vectors (rAAV) are a powerful tool for gene delivery but have a limited DNA carrying capacity. Efforts to expand this genetic payload have focused on engineering the vector components, such as dual trans-splicing vectors which double the delivery size by exploiting the natural concatenation of rAAV genomes in host nuclei. We hypothesized that inefficient dual vector transduction could be improved by modulating host factors which affect concatenation. Since factors mediating concatenation are not well defined, we performed a genome-wide screen to identify host cell regulators. We discover that Homologous Recombination (HR) is inhibitory to dual vector transduction. We demonstrate that depletion or inhibition of HR factors BRCA1 and Rad51 significantly increase reconstitution of a large split transgene by increasing both concatenation and expression from rAAVs. Our results define roles for DNA damage repair in rAAV transduction and highlight the potential for pharmacological intervention to increase genetic payload of rAAV vectors.https://doi.org/10.1038/s41467-025-56738-5
spellingShingle Anna C. Maurer
Brian Benyamini
Oscar N. Whitney
Vinson B. Fan
Claudia Cattoglio
Djem U. Kissiov
Gina M. Dailey
Xavier Darzacq
Matthew D. Weitzman
Robert Tjian
Double-strand break repair pathways differentially affect processing and transduction by dual AAV vectors
Nature Communications
title Double-strand break repair pathways differentially affect processing and transduction by dual AAV vectors
title_full Double-strand break repair pathways differentially affect processing and transduction by dual AAV vectors
title_fullStr Double-strand break repair pathways differentially affect processing and transduction by dual AAV vectors
title_full_unstemmed Double-strand break repair pathways differentially affect processing and transduction by dual AAV vectors
title_short Double-strand break repair pathways differentially affect processing and transduction by dual AAV vectors
title_sort double strand break repair pathways differentially affect processing and transduction by dual aav vectors
url https://doi.org/10.1038/s41467-025-56738-5
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