ArticleProceedings of the National Academy of Sciences of the United States of America2017
Contribution of canonical nonhomologous end joining to chromosomal rearrangements is enhanced by ATM kinase deficiency.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 29 citations in OpenAlex.
- 53BP1-RIF1 and DNA-PKcs show distinct genetic interactions with diverse chromosomal break repair outcomes.Nature communications · 2025Article
- Disparate Pathways for Extrachromosomal DNA Biogenesis and Genomic DNA Repair.Cancer discovery · 2025Article
- TREX2 enables efficient genome disruption mediated by paired CRISPR-Cas9 nickases that generate 3'-overhanging ends.Molecular therapy. Nucleic acids · 2023Article
- Prevalence and mechanisms of somatic deletions in single human neurons during normal aging and in DNA repair disorders.Nature communications · 2022Article
- To indel or not to indel: Factors influencing mutagenesis during chromosomal break end joining.DNA repair · 2022Review
- Cas9 exo-endonuclease eliminates chromosomal translocations during genome editing.Nature communications · 2022Article
- Reconsidering pathway choice: a sequential model of mammalian DNA double-strand break pathway decisions.Current opinion in genetics & development · 2021Review
- Analysis of NHEJ-Based DNA Repair after CRISPR-Mediated DNA Cleavage.International journal of molecular sciences · 2021Article
- Origin, Regulation, and Fitness Effect of Chromosomal Rearrangements in the YeastInternational journal of molecular sciences · 2021Review
- Genomic Reporter Constructs to Monitor Pathway-Specific Repair of DNA Double-Strand Breaks.Frontiers in genetics · 2021Review
- A robust CRISPR-Cas9-based fluorescent reporter assay for the detection and quantification of DNA double-strand break repair.Nucleic acids research · 2020Article
- RNF8 has both KU-dependent and independent roles in chromosomal break repair.Nucleic acids research · 2020Article
- The RAD52 S346X variant reduces risk of developing breast cancer in carriers of pathogenic germline BRCA2 mutations.Molecular oncology · 2020Article
- The canonical non-homologous end joining factor XLF promotes chromosomal deletion rearrangements in human cells.The Journal of biological chemistry · 2020Article
- Low dose ionizing radiation strongly stimulates insertional mutagenesis in a γH2AX dependent manner.PLoS genetics · 2020Article
- Can Designer Indels Be Tailored by Gene Editing?: Can Indels Be Customized?BioEssays : news and reviews in molecular, cellular and developmental biology · 2019Article
- DNA methylation at an enhancer of the three prime repair exonuclease 2 gene (TREX2) is linked to gene expression and survival in laryngeal cancer.Clinical epigenetics · 2019Article
- Predicting the mutations generated by repair of Cas9-induced double-strand breaks.Nature biotechnology · 2018Article
- Kinase-dependent structural role of DNA-PKcs during immunoglobulin class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Exposure to galactic cosmic radiation compromises DNA repair and increases the potential for oncogenic chromosomal rearrangement in bronchial epithelial cells.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
A likely mechanism of chromosomal rearrangement formation involves joining the ends from two different chromosomal double-strand breaks (DSBs). These events could potentially be mediated by either of two end-joining (EJ) repair pathways [canonical nonhomologous end joining (C-NHEJ) or alternative end joining (ALT-EJ)], which cause distinct rearrangement junction patterns. The relative role of these EJ pathways during rearrangement formation has remained controversial. Along these lines, we have tested whether the DNA damage response mediated by the Ataxia Telangiectasia Mutated (ATM) kinase may affect the relative influence of C-NHEJ vs. ALT-EJ on rearrangement formation. We developed a reporter in mouse cells for a 0.4-Mbp deletion rearrangement that is formed by EJ between two DSBs induced by the Cas9 endonuclease. We found that disruption of the ATM kinase causes an increase in the frequency of the rearrangement as well as a shift toward rearrangement junctions that show hallmarks of C-NHEJ. Furthermore, ATM suppresses rearrangement formation in an experimental condition, in which C-NHEJ is the predominant EJ repair event (i.e., expression of the 3' exonuclease Trex2). Finally, several C-NHEJ factors are required for the increase in rearrangement frequency caused by inhibition of the ATM kinase. We also examined ATM effectors and found that H2AX shows a similar influence as ATM, whereas the influence of ATM on this rearrangement seems independent of 53BP1. We suggest that the contribution of the C-NHEJ pathway to the formation of a 0.4-Mbp deletion rearrangement is enhanced in ATM-deficient cells.
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