ArticlePLoS genetics2010
ATM limits incorrect end utilization during non-homologous end joining of multiple chromosome breaks.
Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 46 citations in OpenAlex.
- iMUT-seq: high-resolution DSB-induced mutation profiling reveals prevalent homologous-recombination dependent mutagenesis.Nature communications · 2023Article
- To indel or not to indel: Factors influencing mutagenesis during chromosomal break end joining.DNA repair · 2022Review
- Restoration of DNA repair mitigates genome instability and increases productivity of Chinese hamster ovary cells.Biotechnology and bioengineering · 2022Article
- A robust CRISPR-Cas9-based fluorescent reporter assay for the detection and quantification of DNA double-strand break repair.Nucleic acids research · 2020Article
- Article
- Expanding the CRISPR Toolbox with ErCas12a in Zebrafish and Human Cells.The CRISPR journal · 2019Article
- ATM loss leads to synthetic lethality in BRCA1 BRCT mutant mice associated with exacerbated defects in homology-directed repair.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Contribution of canonical nonhomologous end joining to chromosomal rearrangements is enhanced by ATM kinase deficiency.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Differences in the recruitment of DNA repair proteins at subtelomeric and interstitial I-SceI endonuclease-induced DNA double-strand breaks.DNA repair · 2017Article
- High-Fidelity Reprogrammed Human IPSCs Have a High Efficacy of DNA Repair and Resemble hESCs in Their MYC Transcriptional Signature.Stem cells international · 2016Article
- EEPD1 Rescues Stressed Replication Forks and Maintains Genome Stability by Promoting End Resection and Homologous Recombination Repair.PLoS genetics · 2015Article
- Non-redundant Functions of ATM and DNA-PKcs in Response to DNA Double-Strand Breaks.Cell reports · 2015Article
- Processing by MRE11 is involved in the sensitivity of subtelomeric regions to DNA double-strand breaks.Nucleic acids research · 2015Article
- XRCC4/XLF Interaction Is Variably Required for DNA Repair and Is Not Required for Ligase IV Stimulation.Molecular and cellular biology · 2015Article
- Identification of novel radiosensitizers in a high-throughput, cell-based screen for DSB repair inhibitors.Molecular cancer therapeutics · 2015Article
- DNA damage response factors from diverse pathways, including DNA crosslink repair, mediate alternative end joining.PLoS genetics · 2015Article
- Recombination promoted by DNA viruses: phage λ to herpes simplex virus.Annual review of microbiology · 2014Review
- 53BP1 is limiting for NHEJ repair in ATM-deficient model systems that are subjected to oncogenic stress or radiation.Molecular cancer research : MCR · 2013Article
- Concurrent V(D)J recombination and DNA end instability increase interchromosomal trans-rearrangements in ATM-deficient thymocytes.Nucleic acids research · 2013Article
- The role of ATM in the deficiency in nonhomologous end-joining near telomeres in a human cancer cell line.PLoS genetics · 2013Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Chromosome rearrangements can form when incorrect ends are matched during end joining (EJ) repair of multiple chromosomal double-strand breaks (DSBs). We tested whether the ATM kinase limits chromosome rearrangements via suppressing incorrect end utilization during EJ repair of multiple DSBs. For this, we developed a system for monitoring EJ of two tandem DSBs that can be repaired using correct ends (Proximal-EJ) or incorrect ends (Distal-EJ, which causes loss of the DNA between the DSBs). In this system, two DSBs are induced in a chromosomal reporter by the meganuclease I-SceI. These DSBs are processed into non-cohesive ends by the exonuclease Trex2, which leads to the formation of I-SceI-resistant EJ products during both Proximal-EJ and Distal-EJ. Using this method, we find that genetic or chemical disruption of ATM causes a substantial increase in Distal-EJ, but not Proximal-EJ. We also find that the increase in Distal-EJ caused by ATM disruption is dependent on classical non-homologous end joining (c-NHEJ) factors, specifically DNA-PKcs, Xrcc4, and XLF. We present evidence that Nbs1-deficiency also causes elevated Distal-EJ, but not Proximal-EJ, to a similar degree as ATM-deficiency. In addition, to evaluate the roles of these factors on end processing, we examined Distal-EJ repair junctions. We found that ATM and Xrcc4 limit the length of deletions, whereas Nbs1 and DNA-PKcs promote short deletions. Thus, the regulation of end processing appears distinct from that of end utilization. In summary, we suggest that ATM is important to limit incorrect end utilization during c-NHEJ.
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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.