Single-cell and in vivo profiling reveal heterogeneous and organ-specific CRISPR-Cas9 off-target and translocation outcomes
CRISPR-Cas9 holds promise for treating genetic disease, but rare off-target mutations and structural variants remain as key safety concerns, especially at scales relevant to therapy. Here, we establish workflows to resolve Cas9 off-target activity in vitro at single-cell resolution and in vivo across different tissues. Using clonally expanded electroporated mouse embryos and embryonic stem cells, we reveal that individual cells exhibit unique off-target and translocation profiles, including events missed in bulk analyses. Integrating single-cell editing with chromatin accessibility, transcription, and DNA methylation measurements suggest that sequence-independent features modulate Cas9 access and cleavage, with preferential editing in regions characterized by open chromatin and lower methylation. In Cas9-inducible mouse models, editing analyses reveal organ-distinct off-target spectra, DNA repair pathway usage, indel patterns, and markedly varying translocation propensity between tissues. These findings demonstrate that off-target activity is heterogeneous across cells and context-dependent across organs, motivating sensitive single-cell analyses and organ-specific evaluation in preclinical development to more accurately assess risk and improve the safety of CRISPR-based genomic medicines. CRISPR can treat genetic disease, but unintended DNA changes remain a safety concern. Here, authors show that off-target editing and translocations vary widely between individual cells and organs, motivating the development of more sensitive and organ-specific safety assays for CRISPR therapies.
Authors
- Johan Forsström
- Pınar Akçakaya (ORCID: https://orcid.org/0000-0001-5868-7069)
- Mark A. Behlke (ORCID: https://orcid.org/0000-0002-4218-857X)
- Bastian Schiffthaler (ORCID: https://orcid.org/0000-0002-9771-467X)
- Kerstin Magnell
- Ashley M. Jacobi (ORCID: https://orcid.org/0000-0002-9364-6518)
- Alexandra Madsen (ORCID: https://orcid.org/0000-0002-0563-5334)
- Julia Liz Touza
- Niklas Selfjord (ORCID: https://orcid.org/0009-0008-5628-5849)
- Michelle J. Porritt (ORCID: https://orcid.org/0000-0003-1700-0085)
- Gavin Kurgan (ORCID: https://orcid.org/0000-0002-4047-1427)
- Aikaterini Emmanouilidi (ORCID: https://orcid.org/0000-0001-9431-6900)
- Marcello Maresca (ORCID: https://orcid.org/0000-0003-0796-661X)
- Inken Dillmann (ORCID: https://orcid.org/0000-0003-3773-3446)
- Julia Lindgren (ORCID: https://orcid.org/0000-0002-3566-2069)
- Nordstrom Karl
- Katja Madeyski-Bengtson
- Panagiotis Antoniou (ORCID: https://orcid.org/0000-0002-0111-3897)
- Marta Martínez-Lage (ORCID: https://orcid.org/0000-0001-5535-025X)
- Jonna Hellsten
- Anna-Lena Loyd
- Joseph Collin
- Daniel Jachimowicz
- Mikaela Stahlberg
- Leif Wigge
- Mike Firth
Institutions
- AstraZeneca (United Kingdom) (GB)
- AstraZeneca (Australia) (AU)
- AstraZeneca (Finland) (FI)
- AstraZeneca (Sweden) (SE)
- AstraZeneca (Germany) (DE)
- Integrated DNA Technologies (United States) (US)
Publication Details
- Journal
- Nature Communications
- Published
- 2026-08-26
- DOI
- https://doi.org/10.1038/s41467-026-77144-5
- Primary Topic
- CRISPR and Genetic Engineering
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- AstraZeneca