ArticleCellular and molecular life sciences : CMLS2017
An efficient method to enrich for knock-out and knock-in cellular clones using the CRISPR/Cas9 system.
Article in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Molecular basis of target RNA cleavage by Cas13.Nature communications · 2026Article
- Homozygous editing of multiple genes for accelerated generation of xenotransplantation pigs.Genome research · 2025Article
- Enrichment strategies to enhance genome editing.Journal of biomedical science · 2023Review
- Development of an efficient single-cell cloning and expansion strategy for genome edited induced pluripotent stem cells.Molecular biology reports · 2022Article
- Dissecting the role ofFrontiers in immunology · 2022Article
- Generation of Monoclonal iPSC Lines with Stable Cas9 Expression and High Cas9 Activity.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Fast and Efficient Genome Editing of Human FOXP3Frontiers in immunology · 2021Article
- AAV-mediated FOXG1 gene editing in human Rett primary cells.European journal of human genetics : EJHG · 2020Article
- A Universal Surrogate Reporter for Efficient Enrichment of CRISPR/Cas9-Mediated Homology-Directed Repair in Mammalian Cells.Molecular therapy. Nucleic acids · 2020Article
- Ways of improving precise knock-in by genome-editing technologies.Human genetics · 2019Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clustered Regularly Interspaced Short Palindromic Repeats-associated protein 9 nuclease (CRISPR/Cas9) and Transcription Activator-Like Effector Nucleases (TALENs) are versatile tools for genome editing. Here we report a method to increase the frequency of Cas9-targeted cellular clones. Our method is based on a chimeric construct with a Blasticidin S Resistance gene (bsr) placed out-of-frame by a surrogate target sequence. End joining of the CRISPR/Cas9-induced double-strand break on the surrogate target can place the bsr in frame, thus providing temporary resistance to Blasticidin S: this is used to enrich for cells where Cas9 is active. By this approach, in a real experimental setting, we disrupted the Aicda gene in ~70% of clones from CH12F3 lymphoma cells (>40% biallelically). With the same approach we knocked in a single nucleotide to reconstruct the frame of Aicda in these null cells, restoring the function in ~37% of the clones (less than 10% by the standard approach). Targeting of single nucleotide changes in other genes yielded analogous results. These results support our enrichment method as an efficient tool in genome editing.
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Registered trials
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