ArticleThe Journal of cell biology2011
Cdk1 uncouples CtIP-dependent resection and Rad51 filament formation during M-phase double-strand break repair.
Article in The Journal of cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
62 citing papers in PubMed, 86 citations in OpenAlex.
- CRISPR/Cas9-Based Genome Editing: Understanding Differences in DNA Repair Pathways, Profiles, and Outcomes.International journal of molecular sciences · 2026Review
- Nonhomologous end joining-the importance of end tethering and beyond.Genes & development · 2026Review
- Sae2 integrates CDK and checkpoint phosphorylation to coordinate MRX cleavage with checkpoint attenuation.Communications biology · 2025Article
- DNA double-strand break end resection factors and WRN facilitate mitotic DNA synthesis in human cells.Nature communications · 2025Article
- Mechanisms and regulation of DNA end resection in the maintenance of genome stability.Nature reviews. Molecular cell biology · 2025Review
- CDK1 mediates the metabolic regulation of DNA double-strand break repair in metaphase II oocytes.BMC biology · 2025Article
- A TRilogy of ATR's Non-Canonical Roles Throughout the Cell Cycle and Its Relation to Cancer.Cancers · 2024Review
- 53BP1 deficiency leads to hyperrecombination using break-induced replication (BIR).Nature communications · 2024Article
- 53BP1 deficiency leads to hyperrecombination using break-induced replication (BIR).bioRxiv : the preprint server for biology · 2024Article
- Dbf4-dependent kinase promotes cell cycle controlled resection of DNA double-strand breaks and repair by homologous recombination.Nature communications · 2024Article
- CRISPR/Cas9 system and its applications in nervous system diseases.Genes & diseases · 2024Review
- Modulation of cell cycle increases CRISPR-mediated homology-directed DNA repair.Cell & bioscience · 2023Article
- Article
- CRISPR/Cas9-mediated targeted knock-in of large constructs using nocodazole and RNase HII.Scientific reports · 2023Article
- Processing DNA lesions during mitosis to prevent genomic instability.Biochemical Society transactions · 2022Review
- BRD4 promotes resection and homology-directed repair of DNA double-strand breaks.Nature communications · 2022Article
- NBS1-CtIP-mediated DNA end resection suppresses cGAS binding to micronuclei.Nucleic acids research · 2022Article
- DNA Repair Pathway Choices in CRISPR-Cas9-Mediated Genome Editing.Trends in genetics : TIG · 2021Review
- PIF1 helicase promotes break-induced replication in mammalian cells.The EMBO journal · 2021Article
- Advances and Obstacles in Homology-Mediated Gene Editing of Hematopoietic Stem Cells.Journal of clinical medicine · 2021Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 4 countries.
Funding
Abstract
DNA double-strand break (DSB) resection, which results in RPA-bound single-stranded DNA (ssDNA), is activated in S phase by Cdk2. RPA-ssDNA activates the ATR-dependent checkpoint and homology-directed repair (HDR) via Rad51-dependent mechanisms. On the other hand, the fate of DSBs sustained during vertebrate M phase is largely unknown. We use cell-free Xenopus laevis egg extracts to examine the recruitment of proteins to chromatin after DSB formation. We find that S-phase extract recapitulates a two-step resection mechanism. M-phase chromosomes are also resected in cell-free extracts and cultured human cells. In contrast to the events in S phase, M-phase resection is solely dependent on MRN-CtIP. Despite generation of RPA-ssDNA, M-phase resection does not lead to ATR activation or Rad51 chromatin association. Remarkably, we find that Cdk1 permits resection by phosphorylation of CtIP but also prevents Rad51 binding to the resected ends. We have thus identified Cdk1 as a critical regulator of DSB repair in M phase. Cdk1 induces persistent ssDNA-RPA overhangs in M phase, thereby preventing both classical NHEJ and Rad51-dependent HDR.
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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.