ArticleMolecular cell2008
Differential regulation of the cellular response to DNA double-strand breaks in G1.
Article in Molecular cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.
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Who cites it
110 citing papers in PubMed.
- Dbf4-dependent kinase promotes cell cycle controlled resection of DNA double-strand breaks and repair by homologous recombination.Nature communications · 2024Article
- Article
- Increased Gene Targeting in Hyper-Recombinogenic LymphoBlastoid Cell Lines Leaves Unchanged DSB Processing by Homologous Recombination.International journal of molecular sciences · 2022Article
- Article
- MCMBP promotes the assembly of the MCM2-7 hetero-hexamer to ensure robust DNA replication in human cells.eLife · 2022Article
- Complex Mechanisms of Antimony Genotoxicity in Budding Yeast Involves Replication and Topoisomerase I-Associated DNA Lesions, Telomere Dysfunction and Inhibition of DNA Repair.International journal of molecular sciences · 2021Article
- Review
- DNA damage triggers increased mobility of chromosomes in G1-phase cells.Molecular biology of the cell · 2019Article
- An Assay to Study Intra-Chromosomal Deletions in Yeast.Methods and protocols · 2019Article
- KEOPS complex promotes homologous recombination via DNA resection.Nucleic acids research · 2019Article
- Chromatin mobility upon DNA damage: state of the art and remaining questions.Current genetics · 2019Review
- Article
- Article
- Cell cycle-dependent spatial segregation of telomerase from sites of DNA damage.The Journal of cell biology · 2017Article
- DNA Damage Induces a Secretory Program in the Quiescent TME that Fosters Adverse Cancer Phenotypes.Molecular cancer research : MCR · 2017Article
- Article
- A game of musical chairs: Pro- and anti-resection factors compete for TOPBP1 binding after DNA damage.The Journal of cell biology · 2017Article
- Article
- The yeast Aft2 transcription factor determines selenite toxicity by controlling the low affinity phosphate transport system.Scientific reports · 2016Article
- The structure of ends determines the pathway choice and Mre11 nuclease dependency of DNA double-strand break repair.Nucleic acids research · 2016Article
50 more citing papers are in PubMed but not listed here.
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3 authors.
Funding
Abstract
Double-strand breaks (DSBs) are potentially lethal DNA lesions that can be repaired by either homologous recombination (HR) or nonhomologous end-joining (NHEJ). We show that DSBs induced by ionizing radiation (IR) are efficiently processed for HR and bound by Rfa1 during G1, while endonuclease-induced breaks are recognized by Rfa1 only after the cell enters S phase. This difference is dependent on the DNA end-binding Yku70/Yku80 complex. Cell-cycle regulation is also observed in the DNA damage checkpoint response. Specifically, the 9-1-1 complex is required in G1 cells to recruit the Ddc2 checkpoint protein to damaged DNA, while, upon entry into S phase, the cyclin-dependent kinase Cdc28 and the 9-1-1 complex both serve to recruit Ddc2 to foci. Together, these results demonstrate that the DNA repair machinery distinguishes between different types of damage in G1, which translates into different modes of checkpoint activation in G1 and S/G2 cells.
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