ArticleMolecular cell2015
Mre11-Sae2 and RPA Collaborate to Prevent Palindromic Gene Amplification.
Article in Molecular cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
43 citing papers in PubMed, 69 citations in OpenAlex.
- Lesions initiating spontaneous mitotic crossover are minimally subject to non-homologous end joining.bioRxiv : the preprint server for biology · 2026Article
- The bacterial MRE11-RAD50 and DNA2-WRN homologs process replication forks at distinct and separate loci on the chromosome.FEBS letters · 2026Article
- Overcoming natural replication barriers formed by DNA structures and the role of repositioning to the nuclear periphery.DNA repair · 2025Review
- Sae2 controls Mre11 endo- and exonuclease activities by different mechanisms.Nature communications · 2024Article
- ATR limits Rad18-mediated PCNA monoubiquitination to preserve replication fork and telomerase-independent telomere stability.The EMBO journal · 2024Article
- Double-strand breaks induce inverted duplication chromosome rearrangements by a DNA polymerase δ-dependent mechanism.Nature communications · 2023Article
- Widely spaced and divergent inverted repeats become a potent source of chromosomal rearrangements in long single-stranded DNA regions.Nucleic acids research · 2023Article
- Chromatin accessibility: methods, mechanisms, and biological insights.Nucleus (Austin, Tex.) · 2022Review
- Article
- DNA end resection during homologous recombination.Current opinion in genetics & development · 2021Review
- Palindromes in DNA-A Risk for Genome Stability and Implications in Cancer.International journal of molecular sciences · 2021Review
- MRN complex is an essential effector of DNA damage repair.Journal of Zhejiang University. Science. B · 2021Review
- Origin, Regulation, and Fitness Effect of Chromosomal Rearrangements in the YeastInternational journal of molecular sciences · 2021Review
- The fragility of a structurally diverse duplication block triggers recurrent genomic amplification.Nucleic acids research · 2021Article
- Exploiting the Microhomology-Mediated End-Joining Pathway in Cancer Therapy.Cancer research · 2020Review
- Mechanisms underlying genome instability mediated by formation of foldback inversions ineLife · 2020Article
- Expandable and reversible copy number amplification drives rapid adaptation to antifungal drugs.eLife · 2020Article
- Loss of Cdc13 causes genome instability by a deficiency in replication-dependent telomere capping.PLoS genetics · 2020Article
- CDK and Mec1/Tel1-catalyzed phosphorylation of Sae2 regulate different responses to DNA damage.Nucleic acids research · 2019Article
- EssentialProceedings of the National Academy of Sciences of the United States of America · 2019Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Foldback priming at DNA double-stranded breaks is one mechanism proposed to initiate palindromic gene amplification, a common feature of cancer cells. Here, we show that small (5-9 bp) inverted repeats drive the formation of large palindromic duplications, the major class of chromosomal rearrangements recovered from yeast cells lacking Sae2 or the Mre11 nuclease. RPA dysfunction increased the frequency of palindromic duplications in Sae2 or Mre11 nuclease-deficient cells by ∼ 1,000-fold, consistent with intra-strand annealing to create a hairpin-capped chromosome that is subsequently replicated to form a dicentric isochromosome. The palindromic duplications were frequently associated with duplication of a second chromosome region bounded by a repeated sequence and a telomere, suggesting the dicentric chromosome breaks and repairs by recombination between dispersed repeats to acquire a telomere. We propose secondary structures within single-stranded DNA are potent instigators of genome instability, and RPA and Mre11-Sae2 play important roles in preventing their formation and propagation, respectively.
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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.