ArticleNature communications2024
Uncovering the dynamics of precise repair at CRISPR/Cas9-induced double-strand breaks.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Distinct repair outcomes from single and convergent replication fork collapse.Nature structural & molecular biology · 2026Article
- Both genome instability and replicative senescence stem from the shortest telomere in telomerase-negative cells.Nature communications · 2026Article
- Influence of gRNA efficiency and inversion size on the frequency of CRISPR/Cas9-induced chromosomal inversions in tomato protoplasts.BMC plant biology · 2026Article
- Features affecting Cas9-induced editing efficiency and patterns in tomato: evidence from a large CRISPR dataset.The Plant journal : for cell and molecular biology · 2026Article
- Conformational dynamics of CRISPR-Cas type I-F-HNH inform nickase engineering in a cascade scaffold.Nucleic acids research · 2026Article
- Plant tolerance mechanisms to DNA-damaging UV stress.Journal of experimental botany · 2025Review
- The Potential of NGTs to Overcome Constraints in Plant Breeding and Their Regulatory Implications.International journal of molecular sciences · 2025Review
- A CRISPR/Cas9-induced restoration of bioluminescence reporter system for single-cell gene expression analysis in plants.Scientific reports · 2025Article
- Unveiling the cut-and-repair cycle of designer nucleases in human stem and T cells via CLEAR-time dPCR.Nature communications · 2025Article
- The multiple layers of RNA response in double-strand break repair.Experimental & molecular medicine · 2025Review
- CRISPR/Cas9 generated DSB clusters mimic complex lesions induced by high-LET radiation and shift repair from c-NHEJ to mutagenic repair pathways.Scientific reports · 2025Article
- Proposed EU NGT legislation in light of plant genetic variation.Plant biotechnology journal · 2025Review
- Characterization of radiations-induced genomic structural variations in Arabidopsis thaliana.The Plant journal : for cell and molecular biology · 2025Article
- CRISPR-epigenetic crosstalk: From bidirectional regulation to therapeutic potential.Computational and structural biotechnology journal · 2025Review
- RAD52 and ERCC6L/PICH have a compensatory relationship for genome stability in mitosis.PLoS genetics · 2024Article
- Investigating Inherited Heart Diseases Using Human Induced Pluripotent Stem Cell-Based Models.Life (Basel, Switzerland) · 2024Review
- Widespread position-dependent transcriptional regulatory sequences in plants.Nature genetics · 2024Article
- Dual activities of an X-family DNA polymerase regulate CRISPR-induced insertional mutagenesis across species.Nature communications · 2024Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
CRISPR/Cas9 is widely used for precise mutagenesis through targeted DNA double-strand breaks (DSBs) induction followed by error-prone repair. A better understanding of this process requires measuring the rates of cutting, error-prone, and precise repair, which have remained elusive so far. Here, we present a molecular and computational toolkit for multiplexed quantification of DSB intermediates and repair products by single-molecule sequencing. Using this approach, we characterize the dynamics of DSB induction, processing and repair at endogenous loci along a 72 h time-course in tomato protoplasts. Combining this data with kinetic modeling reveals that indel accumulation is determined by the combined effect of the rates of DSB induction processing of broken ends, and precise versus error repair. In this study, 64-88% of the molecules were cleaved in the three targets analyzed, while indels ranged between 15-41%. Precise repair accounts for most of the gap between cleavage and error repair, representing up to 70% of all repair events. Altogether, this system exposes flux in the DSB repair process, decoupling induction and repair dynamics, and suggesting an essential role of high-fidelity repair in limiting the efficiency of CRISPR-mediated mutagenesis.
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