ArticleNucleic acids research2020
CRISPR/Cas9 treatment causes extended TP53-dependent cell cycle arrest in human cells.
Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 46 citations in OpenAlex.
- Perspective on Lessons Not Learned: From Coley's Toxins to Microbial Drug Delivery, Guidance for Institutional Review Boards (IRBs).International journal of molecular sciences · 2026Review
- Restoration of the immune system with base editing and non-genotoxic conditioning in a Rag2 point-mutant mouse model.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Modalities of vision restoration in optic neuropathies and retinal disease.Progress in retinal and eye research · 2026Review
- Prime editing-mediated microhomology enables efficient replacement of large DNA.Nucleic acids research · 2026Article
- Non-viral targeted integration of large DNA in primary human T cells independent of double-stranded DNA breaks.Nature biomedical engineering · 2026Article
- Enhancement of prime editing by recruiting engineered or evolved components and implementing novel strategies.Biochemistry and biophysics reports · 2026Review
- Illuminating the genome: emerging approaches in CRISPR-Cas live-cell imaging.Nucleic acids research · 2026Review
- Challenges in visualizing endogenousBiotechnologia · 2026Review
- Mutations in the β-tubulin TUBB impair ciliogenesis and are associated with ciliopathy-like phenotypes.Nature communications · 2025Article
- Unveiling the cut-and-repair cycle of designer nucleases in human stem and T cells via CLEAR-time dPCR.Nature communications · 2025Article
- A CRISPR-Cas9-based system for the dose-dependent study of DNA double-strand break sensing and repair.The FEBS journal · 2025Article
- Live genome imaging by CRISPR engineering: progress and problems.Experimental & molecular medicine · 2025Review
- Transcriptome analysis reveals no obvious unintended effects in the spleen of CRISPR/Cas9-mediated CD163 and pAPN double-knockout pigs.Functional & integrative genomics · 2025Article
- Article
- Precise kilobase-scale genomic insertions in mammalian cells using PASTE.Nature protocols · 2025Review
- Prime Editing: A Revolutionary Technology for Precise Treatment of Genetic Disorders.Cell proliferation · 2025Review
- TP53 mutations in cancer: Molecular features and therapeutic opportunities (Review).International journal of molecular medicine · 2025Review
- Computationally guided high-throughput engineering of an anti-CRISPR protein for precise genome editing in human cells.Cell reports methods · 2024Article
- AMPK/MTOR/TP53 Signaling Pathway Regulation by Calcitonin Gene-Related Peptide Reduces Oxygen-Induced Lung Damage in Neonatal Rats through Autophagy Promotion.Inflammation · 2024Article
- Evaluation of guide-free Cas9-induced genomic damage and transcriptome changes in pig embryos.Molecular therapy. Nucleic acids · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
While the mechanism of CRISPR/Cas9 cleavage is understood, the basis for the large variation in mutant recovery for a given target sequence between cell lines is much less clear. We hypothesized that this variation may be due to differences in how the DNA damage response affects cell cycle progression. We used incorporation of EdU as a marker of cell cycle progression to analyze the response of several human cell lines to CRISPR/Cas9 treatment with a single guide directed to a unique locus. Cell lines with functionally wild-type TP53 exhibited higher levels of cell cycle arrest compared to lines without. Chemical inhibition of TP53 protein combined with TP53 and RB1 transcript silencing alleviated induced arrest in TP53+/+ cells. Using dCas9, we determined this arrest is driven in part by Cas9 binding to DNA. Additionally, wild-type Cas9 induced fewer 53BP1 foci in TP53+/+ cells compared to TP53-/- cells and DD-Cas9, suggesting that differences in break sensing are responsible for cell cycle arrest variation. We conclude that CRISPR/Cas9 treatment induces a cell cycle arrest dependent on functional TP53 as well as Cas9 DNA binding and cleavage. Our findings suggest that transient inhibition of TP53 may increase genome editing recovery in primary and TP53+/+ cell lines.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.