ArticlePLoS genetics2015
Sae2 Function at DNA Double-Strand Breaks Is Bypassed by Dampening Tel1 or Rad53 Activity.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 59 citations in OpenAlex.
- A Tel1-Rad9 axis links DNA double-strand break end-tethering to repair pathway choice.Nucleic acids research · 2026Article
- Engineering yeast chromosomal telomeres with a bacteriophage system.Nature communications · 2026Article
- Sae2 integrates CDK and checkpoint phosphorylation to coordinate MRX cleavage with checkpoint attenuation.Communications biology · 2025Article
- Article
- Mms22-Rtt107 axis attenuates the DNA damage checkpoint and the stability of the Rad9 checkpoint mediator.Nature communications · 2025Article
- Functional and molecular insights into the role of Sae2 C-terminus in the activation of MRX endonuclease.Nucleic acids research · 2024Article
- Exo1 cooperates with Tel1/ATM in promoting recombination events at DNA replication forks.iScience · 2024Article
- Proteasome-mediated degradation of long-range nucleases negatively regulates resection of DNA double-strand breaks.iScience · 2024Article
- Multi-step control of homologous recombination via Mec1/ATR suppresses chromosomal rearrangements.The EMBO journal · 2024Article
- The Mms22-Rtt107 axis dampens the DNA damage checkpoint by reducing the stability of the Rad9 checkpoint mediator.Research square · 2024Article
- The Ku complex promotes DNA end-bridging and this function is antagonized by Tel1/ATM kinase.Nucleic acids research · 2023Article
- Nej1 interacts with Sae2 at DNA double-stranded breaks to inhibit DNA resection.The Journal of biological chemistry · 2022Article
- Dpb4 promotes resection of DNA double-strand breaks and checkpoint activation by acting in two different protein complexes.Nature communications · 2021Article
- Sae2 and Rif2 regulate MRX endonuclease activity at DNA double-strand breaks in opposite manners.Cell reports · 2021Article
- The Srs2 helicase dampens DNA damage checkpoint by recycling RPA from chromatin.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Yeast ATM and ATR kinases use different mechanisms to spread histone H2A phosphorylation around a DNA double-strand break.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Rad9/53BP1 promotes DNA repair via crossover recombination by limiting the Sgs1 and Mph1 helicases.Nature communications · 2020Article
- Checkpoint Responses to DNA Double-Strand Breaks.Annual review of biochemistry · 2020Review
- CtIP promotes the motor activity of DNA2 to accelerate long-range DNA end resection.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Modeling cancer genomic data in yeast reveals selection against ATM function during tumorigenesis.PLoS genetics · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The MRX complex together with Sae2 initiates resection of DNA double-strand breaks (DSBs) to generate single-stranded DNA (ssDNA) that triggers homologous recombination. The absence of Sae2 not only impairs DSB resection, but also causes prolonged MRX binding at the DSBs that leads to persistent Tel1- and Rad53-dependent DNA damage checkpoint activation and cell cycle arrest. Whether this enhanced checkpoint signaling contributes to the DNA damage sensitivity and/or the resection defect of sae2Δ cells is not known. By performing a genetic screen, we identify rad53 and tel1 mutant alleles that suppress both the DNA damage hypersensitivity and the resection defect of sae2Δ cells through an Sgs1-Dna2-dependent mechanism. These suppression events do not involve escaping the checkpoint-mediated cell cycle arrest. Rather, defective Rad53 or Tel1 signaling bypasses Sae2 function at DSBs by decreasing the amount of Rad9 bound at DSBs. As a consequence, reduced Rad9 association to DNA ends relieves inhibition of Sgs1-Dna2 activity, which can then compensate for the lack of Sae2 in DSB resection and DNA damage resistance. We propose that persistent Tel1 and Rad53 checkpoint signaling in cells lacking Sae2 increases the association of Rad9 at DSBs, which in turn inhibits DSB resection by limiting the activity of the Sgs1-Dna2 resection machinery.
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