ArticlePLoS genetics2013
Budding yeast ATM/ATR control meiotic double-strand break (DSB) levels by down-regulating Rec114, an essential component of the DSB-machinery.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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Who cites it
90 citing papers in PubMed, 134 citations in OpenAlex.
- Biomarkers Associating with PARP Inhibitor Benefit in Prostate Cancer in the TOPARP-B Trial.Cancer discovery · 2021Trial
- Controlling Meiotic Double-Strand Break Formation in Mice: A Web of Multivalent Protein-Protein Interactions.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Tuning Meiotic Checkpoints: Evolutionary Costs and Mechanistic Trade-Offs.Annual review of genetics · 2026Review
- Nucleolar Cdc14 Splitting Reflects Recombination Context and Meiotic Chromosome Dynamics.International journal of molecular sciences · 2026Article
- Mutual, spatially limited control of meiotic DNA break formation by Mre11-Rad50-Nbs1 DNA repair complex and Tel1 (ATM) protein kinase.Nucleic acids research · 2025Article
- Tel1 is recruited at chromosomal loop/axis contact sites to modulate meiotic DNA double-strand breaks interference.PLoS genetics · 2025Article
- Insight into meiotic DNA end resection: Mechanisms and regulation.DNA repair · 2025Review
- Rad51, Rad54, and ZMM proteins antagonize the mismatch repair system to promote fertility of budding yeast intraspecies hybrid zygotes.Nucleic acids research · 2025Article
- Spo11: from topoisomerase VI to meiotic recombination initiator.Biochemical Society transactions · 2025Review
- The plant early recombinosome: a high security complex to break DNA during meiosis.Plant reproduction · 2024Review
- Separable roles of the DNA damage response kinase Mec1ATR and its activator Rad24RAD17 during meiotic recombination.PLoS genetics · 2024Article
- Decoding the Nucleolar Role in Meiotic Recombination and Cell Cycle Control: Insights into Cdc14 Function.International journal of molecular sciences · 2024Review
- Seeding the meiotic DNA break machinery and initiating recombination on chromosome axes.Nature communications · 2024Article
- Meiotic prophase length modulates Tel1-dependent DNA double-strand break interference.PLoS genetics · 2024Article
- The molecular machinery of meiotic recombination.Biochemical Society transactions · 2024Review
- SPO-Seq: An Accessible Method for Efficient Evaluation of Spo11 Catalytic Activity and Profiling Meiotic DSB Hotspots in Saccharomyces cerevisiae.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Recombinase-independent chromosomal rearrangements between dispersed inverted repeats in Saccharomyces cerevisiae meiosis.Nucleic acids research · 2023Article
- Structure and DNA-bridging activity of the essential Rec114-Mei4 trimer interface.Genes & development · 2023Article
- Structure and DNA bridging activity of the essential Rec114â€"Mei4 trimer interface.bioRxiv : the preprint server for biology · 2023Article
- The Msh5 complex shows homeostatic localization in response to DNA double-strand breaks in yeast meiosis.Frontiers in cell and developmental biology · 2023Article
30 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 5 institutions in 3 countries.
Funding
Abstract
An essential feature of meiosis is Spo11 catalysis of programmed DNA double strand breaks (DSBs). Evidence suggests that the number of DSBs generated per meiosis is genetically determined and that this ability to maintain a pre-determined DSB level, or "DSB homeostasis", might be a property of the meiotic program. Here, we present direct evidence that Rec114, an evolutionarily conserved essential component of the meiotic DSB-machinery, interacts with DSB hotspot DNA, and that Tel1 and Mec1, the budding yeast ATM and ATR, respectively, down-regulate Rec114 upon meiotic DSB formation through phosphorylation. Mimicking constitutive phosphorylation reduces the interaction between Rec114 and DSB hotspot DNA, resulting in a reduction and/or delay in DSB formation. Conversely, a non-phosphorylatable rec114 allele confers a genome-wide increase in both DSB levels and in the interaction between Rec114 and the DSB hotspot DNA. These observations strongly suggest that Tel1 and/or Mec1 phosphorylation of Rec114 following Spo11 catalysis down-regulates DSB formation by limiting the interaction between Rec114 and DSB hotspots. We also present evidence that Ndt80, a meiosis specific transcription factor, contributes to Rec114 degradation, consistent with its requirement for complete cessation of DSB formation. Loss of Rec114 foci from chromatin is associated with homolog synapsis but independent of Ndt80 or Tel1/Mec1 phosphorylation. Taken together, we present evidence for three independent ways of regulating Rec114 activity, which likely contribute to meiotic DSBs-homeostasis in maintaining genetically determined levels of breaks.
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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.